Drug List – Autonomics and Cardiovascular

CHOLINERGIC DRUGS Muscarinic Agonists – ch. 4 1. Pilocarpine – Eye (M3): topical application produces rapid miosis and contraction of ciliary muscle  accommodation and loss of far vision. One of the most potent stimulators of secretions (sweat, tears, saliva, etc.) but is non-specific a. Clinical use: DOC for glaucoma  lowering intraocular pressure of both narrow-angle (closed angle) and wide angle (open angle) glaucoma b. Side Effects: can enter the brain and cause CNS disturbances; stimulates profuse sweating and salivation. Stinging and local irritation as well 2. Bethanecol – directly stimulates muscarinic receptors, causing ↑ intestinal motility and tone. Also stimulates the detrusor muscles of the bladder, but not the trigone and sphincter  expulsion of urine. PO, renal excretion, not degraded by cholinesterase a. Clinical: stimulates atonic bladder (particularly in non-obstructive urinary retention) b. Side effects: generalized cholinergic stimulation including: sweating, salivation, flushing, ↓ BP, nausea, abdominal pain, diarrhea, bronchospasm, and miosis. c. Contraindications: asthmatics (due to bronchoconstriction) 3. Carbachol – has both muscarinic and nicotinic actions. Effects both the CV system and the GI system because of its ganglion-stimulating activity, may stimulate then depress these systems. Can cause epinephrine release from the adrenal medulla by nicotinic action. In the eye, it mimics the effects of ACh  miosis a. Clinical: glaucoma treatment in the eye as a miotic agent by causing papillary constriction  ↓ intraocular pressure b. Side effects: none when used ophthamalogically Anticholinesterases – ch. 4 4. Physostigmine – has cholinergic, nicotinic, and muscarinic actions. It is a cholinesterase inhibitor, but is also a tertiary amine and therefore can cross the BBB. a. Clinical: ↑ intestinal and bladder motility for atony. In the eye  miosis and spasm of accommodation (glaucoma). Also used to treat overdoses of anticholinergics (atropine, phenothiazine, and tricyclic anti-depressants) b. Side effects: convulsions, respiratory and cardiovascular depression. Possible paralysis of skeletal muscle, but rare in therapeutic doses 5. Neostigmine – cholinesterase inhibitor carbamylates cholinesterase’s active site making the enzyme resistant to hydration (preventing activation)  accumulation of ACh at the neuromuscular junction. Bowel and bladder smooth muscle: causes ↑ tone, ↑ motility, sphincter relaxation. Skeletal muscle: reverses nondepolarizing (i.e. competitive) neuromuscular blockade. Also used for sympathetic and parasympathetic stimulation of the heart (parasympathetic dominates). Effects last 30min – 2hr



7. 8.


a. Clinical: ↑ GI motility, stimulates bladder contraction (in atony), treats myasthenia gravis[MG] (degrades the nicotinic receptors at the neuromuscular junction so there are fewer receptors that get attacked by the autoimmune antibodies of MG) b. Side effects: general cholinergic stimulation (salivation, flushing, ↓d BP, nausea, abdominal pain, diarrhea, bronchospasm) Edrophonium – Reversibly binds ACh-esterase at the neuromuscular junction (NMJ). Short acting (10-20min), IV, renal excretion, inactivated by plasma esterases a. Clinical: Used to diagnose MG but not treat it because it is too short acting. i. Tensilon Test: ↑ ACh at NMJ can overcome ACh receptor ab’s  sudden, short-lasting improvement followed by ↓d muscle strength ii. Used to differentiate worsening MG vs. overmedication  will make overmedication worse, but will improve worsening MG Pyridostigmine – similar to edrophonium. Has a long half-life and is used mainly for treatment of myasthenia gravis Isoflurophate (DFP) – an organophosphate that covalently binds to a serine-OH at the active site of ACh-esterase  permanent inactivation of ACh-esterase. Restoration of ACh-esterase activity requires synthesis of new ACh-esterase. a. Clinical: Ophthalmic ointment used for chronic treatment of open-angle glaucoma. Effects can last up to a week b. Actions: generalized cholinergic stimulation, paralysis of motor functions  breathing difficulties; convulsions, intense miosis Pralidoxime (2-PAM) – reactivates inhibited ACh-esterase, but is unable to go into the CNS. It can displace organophosphates like isoflurophate as long as aging (loss of the alkyl group  irreversible binding) hasn’t occurred a. Clinical: Used to treat overdose of ambenonium, neostigmine, and pyridostigmine that are used to treat myasthenia gravis. Usually used in combination with atropine to offset effects of DFP

Muscarinic Antagonists – ch. 5 10. Atropine – a tertiary amine belladonna alkaloid that acts competitively on muscarinic receptors in CNS and PNS (parasympathetics)  prevents ACh binding to muscarinic receptors a. Clinical: Treatment of bradycardia. i. Cholinesterase inhibitor overdose  treats bradycardias caused by vagal hyperactivity ii. Ophthalmic  causes cycloplegia (paralysis of ciliary muscle) and mydriasis (pupil dilation) iii. GU: treatment of cramping and urgent bladder in mild cystitis. Reduces hypermotility of bladder iv. Low dose: ↓ saliva, ↓ bronchial secretion, ↓ sweat v. Med. Dose: mydriasis, cycloplegia, ↑ HR vi. Large Dose: inhibition of urination; ↓ GI tone, motility, and secretions


b. Side Effects: “red as a beet, blind as a bat, dry as a bone, mad as a hatter.” Dilation of superficial blood vessels  atropine flush; blurred vision; ↓ secretions; hyperthermia; delirium, hallucinations c. Contraindications: Narrow-angle glaucoma (relaxation of iris  obstruction of Schlemm’s canal  ↑ in intraocular pressure) 11. Scopolamine – tertiary amine belladonna alkaloid similar to atropine; has greater action on CNS and longer duration of action in comparison to atropine a. Clinical: used for motion sickness prophylaxis, block of short term memory b. Side Effects: similar to atropine Neuromuscular Blocking Agents – ch. 5 Competitive Blockers 12. Pancuronium – competitive nicotinic receptor antagonist. Produces a nondepolarizing blockade (blocks nicotinic receptors without depolarizing the target cell). At high doses it enters and blocks ion channels at the motor end plate. Drug preferentially blocks nicotinic receptors at motor end plates over nicotinic receptors at autonomic ganglia. This results in surmountable skeletal muscle paralysis. Causes ↑ HR, ↑ CO, blocks NE uptake and stimulates NE release. IV, onset of action is 3-5 min; renal excretion; T1/2 = 12.5 min a. Clinical: Nondepolarizing skeletal muscle relaxant  used as a surgical adjuvant for muscle relaxation b. Side effects: can cause histamine release at higher doses  flushing, edema, erythema, hypotension, tachycardia 13. tubocurarine – the purified active ingredient of curare; is the prototype for nondepolarizing neuromuscular blockers a. Side effects: causes considerable histamine release 14. vecuronium – similar to Pancuronium Depolarizing Agents 15. Succinylcholine – slowly and reversibly binds ACh receptors, causing the channels to open and the neuromuscular membrane to depolarize  causes all receptors to remain in inactive state, prevents response to endogenous ligand binding. Depolarizing blockades are not reversed by cholinesterase inhibitors. Rapidly hydrolyzed by plasma and liver pseudocholinesterases. a. Clinical: Skeletal muscle relaxation for brief surgical procedures. IV drips for longer procedures b. Side effects: Malignant hyperthermia; hypotension, arrhythmias, respiratory collapse; ↑ intraocular pressure


ADRENERGIC DRUGS Alpha Adrenergic Agonists – ch. 6 16. Norepinephrine (NE) – selectively stimulates α1, α2, β1-adrenoreceptors (α1 = α2 > β1); no effect on β2. The net effect of NE is peripheral vasoconstriction and ↑ BP +/- ↑ inotropy (contractility). IV, metabolism by MAO (mono-amine oxidase) and COMT (catechol O-methyltransferase) a. α1: (PIP2 cascade)  vascular smooth muscle contraction (↑ SVR systemic vascular resistance); mydriasis (pupillary muscle contraction); pilomotor contraction. b. α2: (Gi, ↓ cAMP)  feedback inhibition of adrenergic NT release c. β1: (Gs, ↓ cAMP)  ↑ HR and inotropy d. Clinical: severe hypotension, septic shock e. Side effects: angina, MI (↑ cardiac work), arrhythmias. Can cause tissue necrosis if it extravasates (to exude from a vessel into surrounding tissue) 17. Phenylephrine α1 – Binds to a-adrenoreceptors, activation of PIP2 cascade  activation of protein kinase C  ↑ intracellular Ca++. Contracts vascular smooth muscle  ↑ systemic vascular resistance  ↑ BP (both systolic and diastolic) a. Clinical: Nasal decongestant - secondary to ↓ volume of nasal mucosa via vascular effects i. mydriatic (pupil dilator) without cycloplegia ii. Pressor b. Side effects: local – transient pain. i. Systemic – hypertension, angina ii. Repeated use as a nasal decongestant  rebound mucosal swelling c. Metabolism: long duration of action because its not inactivated by COMT (its not a catecholamine) 18. methoxamine α1 – direct-acting, synthetic adrenergic drug  ↑ BP by stimulation of α1 receptors in the arterioles  vasoconstriction  ↑ BP a. Clinical: acts on vagus nerve to relieve attacks of PSVT. Also used to overcome hypotension during surgery b. Side effects: hypertensive headache, N/V 19. Metaraminol α1>>β1 - Metaraminol is a parenteral vasopressor agent. It is used to reverse or prevent hypotension that occurs with spinal anesthesia, as adjunctive therapy for hemorrhagic hypotension, for medication-induced or surgical complication of hypotension, and for shock associated with brain damage due to trauma or tumor a. Contraindications: Hypotension secondary to chlorpromazine, MAOIs, cardiovascular disease, hemorrhagic shock, hyperthyroidism, hypertension, malaria, sulfite hypersensitivity. 20. Tetrahydrozoline α1 - stimulates alpha-adrenergic receptors. When applied topically to mucous membranes, tetrahydrozoline causes intense vasoconstriction resulting in shrinkage of the mucous membranes. This action promotes drainage and improves ventilation. Ophthalmic administration causes vasoconstriction of conjunctival blood vessels thereby providing relief from minor eye irritations. a. Clinical: intranasal and ophthalmic topical vasoconstrictor. It is administered intranasally to treat nasal congestion associated with acute or


chronic rhinitis, sinusitis, the common cold, and hay fever and other allergies. Contraindicated in closed-angle glaucoma b. Side effects: transient burning, stinging, dryness of the nasal mucosa, and sneezing. Rebound congestion frequently occurs with prolonged use. Ophthalmic preparation can cause transient stinging on initial instillation and blurring of vision. 21. Clonidine α2 – PO, dermal patch; renal excretion. Activates presynaptic a2adrenceptors on sympathetic neurons. These receptors tell the neuron how much NE is in the synapse and act to down regulate further NE release. Some a2adrenoceptors are postsynaptic on vascular smooth muscle, where there stimulation results in vasoconstriction. When given IV  vasoconstriction and hypertension followed by longer period of hypotension. PO  accumulates in CNS suppression of sympathetic outflow a. Clinical: Antihypertensive. Treatment of opioid withdrawal. Antidiuretic in diabetic patients with autonomic neuropathy b. Side Effects: Dry mouth, sedation, sexual dysfunction. Immediate cessation of therapy can cause rebound hypertensive crisis Alpha Adrenergic Antagonists – ch. 7 22. Phentolamine – IV, IM. Nonselective competitive antagonist of α1adrenoceptors. Weak serotonin (5-HT) receptor blocker and histamine receptor agonist. α-blockade  dilation of vascular smooth muscle  ↓ SVR  ↓ BP a. Clinical: DOC for short-term control of hypertension in patients with pheochromocytoma (benign tumor of the adrenal medulla or the sympathetic nervous
system in which the affected cells secrete increased amounts of epinephrine or norepinephrine). Treatment of sympathomimetic amine OD.

Contraindicated in CAD and peptic ulcer disease b. Side effects: orthostatic hypotension (form of low blood pressure precipitated by
moving from a lying or sitting position to standing up straight. Also called postural hypotension). Reflex tachycardia and arrhythmias. GI stimulation and

exacerbation of peptic ulcer disease due to histamine release. Impotence 23. Tolazoline - similar to phentolamine. Tolazoline has very limited clinical application in the treatment of pulmonary hypertension in newborn infants with respiratory distress syndrome. Its efficacy in this condition is doubtful, and the drug is rarely used. 24. Phenoxybenzamine - long-acting, noncompetitive antagonist at alpha-adrenergic receptors. Like phentolamine, phenoxybenzamine antagonizes both alpha1- and alpha2-receptors. a. Clinical: treatment of sweating, HTN w/ pheochromocytoma; urinary symptoms of BPH; and symptoms of certain peripheral vasospastic conditions such as acrocyanosis, Raynaud's phenomenon, and frostbite 25. Prazosin – reversible α1 antagonist; PO, hepatic metabolism. Blockade of α1 adrenoreceptors on vascular smooth muscle  arteriolar and venous vasodilation  ↓ BP, ↓ venous return. Inhibition of smooth muscle contraction in the prostate  relief of urinary symptoms due to BPH. Low affinity for α2 adrenoreceptors  lack
of reflex tachycardia (α2 blockade  ↑ NE release  β1 stimulation of the heart)

a. Clinical: Hypertension, Benign prostatic hyperplasia (BPH), treatment of Raynaud’s phenomenon (vasospasm  digital ischemia) 5

b. Side effects: orthostatic hypotension, syncope. Dry mouth, nightmares, sexual dysfunction, lethargy Beta Adrenergic Agonists – Ch. 6 26. Isoproterenol β1 and β2 - The net effect is ↑ HR, ↑ contractility  ↑ CO  ↑ pulse pressure. Vasodilation  ↓ diastolic BP  no change in systolic BP. IV, metabolized in liver and other tissues by COMT a. β1: (Gs, ↑ cAMP)  ↑ HR and inotropy b. β2: (Gs, ↓ cAMP)  smooth muscle relaxation; bronchial, vascular, and uterine c. Clinical: used in emergencies to stimulate HR in patients with bradycardia or heart block while awaiting insertion of a pacemaker. Contraindicated in patients at risk for tachyarrhythmias and patients with ischemic heart disease d. Side effects: angina, MI (↑ cardiac work), arrhythmias 27. Dobutamine β1>>β2> α1 - The net effect is ↑ cardiac contractility, ↑ HR  ↑ CO. IV, inactivated by COMT and MAO. Tends to ↓ SVR (systemic vascular
resistance), but overall effect on BP is variable, depends on balance b/t ↑ CO and ↓ SVR. Dobutamine can cause ↓ myocardial O2 demand by ↑ inotropy and ↓ SVR, despite causing ↑ HR

a. β1: (Gs, ↑ cAMP)  ↑ HR and inotropy b. β2: (Gs, ↓ cAMP)  smooth muscle relaxation; bronchial, vascular, and uterine c. α1: (PIP2 cascade)  vascular smooth muscle contraction (↑ SVR); mydriasis (pupillary muscle contraction); pilomotor contraction. d. Clinical: short term ↑ CO in CHF. After 1 week of continuous therapy, downregulation of receptors ↓ efficacy of drug e. Side effects: same as epinephrine, arrhythmias, use with caution in atrial fibrillation; contraindicated in hypotension 28. Albuterol β2>>β1 – Directly activates the B2-adrenoceptor  stimulation of adenylate cyclase  ↑ cAMP, MLCK phosphorylation and inactivation  consequent relaxation of smooth muscle and bronchodilation. PO, nebulized, inhaled; not a substrate for COMT  long-acting a. Clinical: treatment of bronchospasm, asthma, bronchitis, and COPD. Contraindicated in patients with CV disease and hyperthyroidism b. Side effects: skeletal muscle tremor, restlessness, apprehension. Sinus tachycardia, other arrhythmias 29. Terbutaline β2>>β1 - similar to albuterol. Used for treatment of emergency asthma attacks. Suppresses premature labor 30. Metaproterenol β2>>β1 – similar to albuterol Beta Adrenergic Antagonists – ch.6 and ch. 7 31. Propranolol – Nonselective β1 and β2 competitive antagonist (nonselective Beta blocker). PO for angina and HTN; IV for arrhythmias and dissection; hepatic metabolism. a. Cardiac myocytes (B1): ↓ inotropy. Combined with ↓ HR  ↓ CO b. Cardiac conductive tissue (B1): ↓ HR, ↑ refractory period at AV node c. Pulmonary (B2): bronchoconstriction d. Renal: ↓ renin secretion


e. Clinical: treats ischemic heart disease, hypertension, aortic dissection, arrhythmias. Portal HTN  ↓ GI bleeding. Migraine prevention, controls symptoms of essential tremor and stage fright f. Side Effects: sinus bradycardia, AV block, hypotension, CHF. Fatigue, depression, impotence, ↓ libido. ↑ VLDL, ↓ HDL 32. Nadolol – similar to propanolol. Longer half-life, fewer CNS effects 33. Metoprolol – B1 competitive antagonist. Similar mechanisms as propanolol. PO for angina and HTN; IV for arrhythmias and dissection; hepatic metabolism a. Clinical: i. Ischemic heart disease: ↓ angina, improves survival post-MI ii. HTN iii. Aortic dissection: ↓ rate of development of systolic BP ↓ risk of dissection extension iv. Arrhythmias: rate control of atrial fibrillation (abnormal irregular
heart rhythm with chaotic generation of electrical signals in the atria of the heart), atrial flutter (Flutter refers to a rapid vibration or pulsation. The difference between flutter and fibrillation is that flutter is well organized while fibrillation is not); prevents ventricular tachycardia (An abnormally rapid heart rhythm that originates from a ventricle, one of the lower chambers of the heart); stops paroxysmal supraventricular tachycardia (is a rapid heart rate, which occurs from time to time (paroxysmal))

b. Side effects: similar to propanolol. May precipitate bronchospasm (even though its B1 selective, still has some B2 activity) 34. Timolol – nonselective B1 and B2 competitive antagonist. Has the same range of CV effects as propranolol. Given as eye drops  ↓ aqueous humor formation. The lack of local anesthetic activity allows this drug to be used on the eye without fear of allowing lesions to occur on an anesthetized cornea a. Clinical: Glaucoma b. Side effects: see propanolol Alpha and Beta Adrenergic – ch. 6 Agonists 35. Epinephrine – stimulates α1, α 2, β1, β2 adrenoreceptors (β predominant at low doses, α at high doses). The net effect is equivalent to sympathetic stimulation: ↑ BP, ↑ HR, ↑ CO, ↓ secretions, ↓ blood flow to splanchnic beds, bronchodilation, and mydriasis. ↑ HR and inotropy  ↑ SV  ↑ systolic BP; vasodilation  ↓ diastolic BP. Higher doses  stimulates α-adrenoreceptors  ↑ systolic and diastolic BP. IV, inactivated by COMT and MAO a. α1: (PIP2 cascade)  vascular smooth muscle contraction (↑ SVR); mydriasis (pupillary muscle contraction); pilomotor contraction. b. α2: (Gi, ↓ cAMP)  feedback inhibition of adrenergic NT release c. β1: (Gs, ↑ cAMP)  ↑ HR and inotropy d. β2: (Gs, ↓ cAMP)  smooth muscle relaxation; bronchial, vascular, and uterine e. Clinical: severe hypotension, cardiogenic shock, anaphylaxis, cardiac arrest, severe bronchospasm. Nasal decongestant; ophthalmic


vasoconstrictor and mydriatic. Used in conjunction with local anesthetic to prolong anesthesia (↓ washout) f. Side effects: angina, MI (↑ cardiac work), arrhythmias g. Contraindications: narrow-angle glaucoma; pregnancy; coronary insufficiency. Don’t use in peripheral IV infusion or inject into fingers, toes, ears, nose  vasoconstriction may cause necrosis 36. Dopamine (D> β>α) – Endogenous catecholamine; IV inactivated by COMT and MAO. Low doses  D1 predominates (↑ renal perfusion and diuresis). Medium doses  β1 predominates (↑ CO). High doses  α1 predominates (↑ SVR) a. D1: renal and splanchnic vasodilation b. β1: (Gs, ↑ cAMP)  ↑ HR and inotropy c. β2: (Gs, ↑ cAMP)  smooth muscle relaxation; bronchial, vascular, and uterine d. α1: (PIP2 cascade)  vascular smooth muscle contraction (↑ SVR); mydriasis (pupillary muscle contraction); pilomotor contraction. e. Clinical: DOC for shock. Enhances natriuresis (excretion of excessive amounts of sodium in the urine) in patients with poor renal perfusion. Treatment of decompensated CHF. Treatment of hypotension f. Side effects: arrhythmias 37. Ephedrine β>α – stimulates release of NE from sympathetic neurons; also acts as a direct adrenergic agonist. Potent CNS stimulator. Net effect is ↑ HR, ↑ CO, variably ↑ SVR, ↑ BP, ↓ secretions and bronchodilation. IV, renal excretion a. α1: (PIP2 cascade)  vascular smooth muscle contraction (↑ SVR); mydriasis (pupillary muscle contraction); pilomotor contraction. b. α2: (Gi, ↓ cAMP)  feedback inhibition of adrenergic NT release c. β1: (Gs, ↑ cAMP)  ↑ HR and inotropy d. β2: (Gs, ↓ cAMP)  smooth muscle relaxation; bronchial, vascular, and uterine e. Clinical: Nasal decongestant; orthostatic hypotension; promotes urinary continence. Contraindicated in hypertension, hyperthyroidism, cerebrovascular insufficiency, ischemic heart disease f. Side effects: hypertension, cardiac arrhythmias. CNS effects: insomnia, anxiety, tremors 38. Amphetamine α−β – presynaptic uptake; causes release of endogenous NE. PO, hepatic metabolism a. Clinical: ADHD, obesity, narcolepsy. Contraindicated in insomnia and anorexia nervosa b. Side effects: dependance (drug of abuse); confusion, abusiveness, delirium (bugs crawling on skin), restlessness, dizziness, tremor, hyperreflexia


Agents Affecting Adrenergic Neurotransmitter Metabolism – Ch. 7 39. Cocaine – indirect sympathomimetic potentiates NE > epinepherine by blocking reuptake of catecholamines at adrenergic nerve terminals. CNS: General stimulation  euphoria, dysphoria, followed by depression (depression of medullary centers  death). CV: small doses  bradycardia; moderate doses  tachycardia, vasoconstriction, arrhythmia, MI. Local anesthetic: blocks Na+ ion channels  ↓ nerve fiber conduction. a. Clinical: surface anesthesia b. Side effects: CV (fatal arrhythmias, coronary vasospasm). Turning into Whitney and Bobby 40. Tyramine - an indirect sympathomimetic and is structurally similar to amphetamine. Like most indirect sympathomimetics, tyramine enters the presynaptic neuron through amine uptake pumps. Once inside the neuron, indirect sympathomimetics are capable of releasing presynaptic stores of norepinephrine and to a lesser degree serotonin and dopamine. Tyramine also can displace epinephrine from the adrenal gland 41. Reserpine – a plant alkaloid, blocks Mg++/ATP dependent transport of biochemical amines (NE, dopa, 5HT) from the cytoplasm into storage vesicles in adrenergic nerves  depletion of NE levels in the adrenergic neurons  ↓ sympathetic function because of the ↓ release of NE. Slow onset and long duration a. Clinical: used to treat HTN that fails to respond to other therapies 42. α –methyldopa - a centrally acting antihypertensive agent. It is metabolized to amethyl-norepinephrine in the brain, and this compound is thought to activate central 2 receptors and lower blood pressure in a manner similar to that of clonidine. 43. Guanethidine - an oral, postganglionic adrenergic blocking agent used for the treatment of hypertension including renal hypertension. Causes depletion of norepinephrine in the synapse, thereby reducing total peripheral resistance and blood pressure. a. Side effects: pronounced orthostatic hypotension b. Contraindications/Precautions: Known or suspected pheochromocytoma, congestive heart failure, or use of MAO inhibitors. Breast-feeding, children, pregnancy


CARDIOVASCULAR DRUGS Chapters 16-22 in Lippincott’s Diuretics ch. 22 Osmotic 44. Mannitol – an osmotic diuretic not subject to tubular reabsorption. Its osmotic pull impairs reabsorption of water in the lumen  osmotic diuresis. Drug may inhibit Na+ and Cl- reabsorption in the proximal tubule and the ascending loop of Henle. Must be given parenterally because its poorly absorbed PO a. Clinical: Maintains high urine flow. ↓ Intracranial pressure and/or intraocular pressure through volume depletion. Contraindicated: sever renal failure, sever dehydration b. Side Effects: Hypernatremia (excessive Na in blood). Extracellular volume expansion: drug rapidly distributes into extracelluar compartment and pulls water out of cells  can lead to pulmonary edema Carbonic Anhydrase Inhibitors 45. Acetazolamide – Inhibits carbonic anhydrase (CA), which catalyzes the reaction HCO3-  CO2 + OH- in proximal convoluted tubule. Inhibition of CA  ↓ reabsorption of HCO3  HCO3 diuresis and possible hyperchloremic metabolic acidosis. CA also found in ciliary body of the eye and choroids plexus. Inhibition of CA in eye  ↓ production of aqueous humor and ↑ CSF production. OPO, IV, renal excretion a. Clinical: Treatment of alkalosis. Alkalinization of urine to ↑ excretion of weak acids. Chronic management of glaucoma (via ↓ aqueous humor). Contraindicated in marked hepatic or renal disease; also in hyperchloric acidosis, hyponatremia, hypokalemia b. Side effects: Renal stones (calcium phosphate is less soluble in alkaline urine). Encephalopathy in liver failure patients (due to ↓ ability to excrete nitrogenous waste in alkaline urine) Thiazides 46. Hydrochlorothiazide – Inhibits Na/Cl transporter in early segment of the distal convoluted tubule (DCT). ↑ urinary K+ excretion because reabsorption of this cation is less efficient when there is ↑ Na delivery to the collecting duct. Induces volume depletion  ↑ aldosterone activity and greater urinary K+ loss. In contrast to loop diuretics, Ca++ reabsorption in enhanced (because Ca++ and Na compete for ATP-dependant reabsorption in DCT). Mg++ reabsorption impaired; reasons unclear. a. Clinical: HTN. Edema (e.g. CHF). Diabetes Insipidus (condition
characterized by frequent and heavy urination, excessive thirst and an overall feeling of weakness. This condition may be caused by a defect in the pituitary gland or in the kidney): compensatory ↑ in Na reabsorption in the proximal convoluted

tubule  ↓ delivery to the DCT  less free water  ↓ polyuria. Contraindications: allergy to sulfa’s; ↑ toxicity of lithium b. Side effects: K+ wasting, metabolic alkalosis, hypercalcemia, Mg depletion. Hyponatremia, Hyperuricemia, hyperglycemia 10

Loop Diuretics 47. Furosemide (Lasix) – inhibits NaCl (via Na/K/2Cl cotransporter) reabsorption in the TAL of loop of Henle. PO, IV, renal excretion and hepatic conjugation. T1/2 = 2-3hrs a. ↑ Urinary excretion of K+ because reabsorption of this cation is less efficient in the face of ↑ Na+ delivery to the collecting duct. Induces volume depletion  ↑ aldosterone activity and ↑ urine K+ loss b. ↑ urinary excretion of Mg++ and Ca++ because reabsorption depends on the luminal electropositivity generated by the Na/K/2Cl cotransporter c. ↑ renal blood flow without altering GFR d. Clinical: Edema. ↑ Urine output in acute renal failure (doesn’t treat actual failure though). Hypercalcemia, hyperkalemia. Contraindicated in sulfa allergy patients e. Side effects: K-wasting, metabolic alkalosis, Mg++ depletion. Ototoxicity, hyperuricemia 48. Ethacrynic Acid – similar to furosemide. The only loop diuretic without a sulfa group and therefore can by used by patients allergic to sulfa’s 49. Torsemide – similar to furosemide. Loop diuretic that has roughly equal potency IV and PO K+ Sparing 50. Spironolactone – K+-sparing. Synthetic steroid that is a competitive antagonist of aldosterone at the receptor side in the DCT. Binds to the receptor and prevents it from achieving its active form. Aldosterone enhances Na and K channel activity  ↑ Na absorption and K+ excretion. Drug causes ↑ Ca++ excretion via direct effect on tubular transport a. Clinical: HTN (often added to other diuretic regimens to minimize K+ loss). i. Edema secondary to CHF, cirrhosis, and nephritic syndrome ii. Primary hyperaldosteronism b. Side effects: Hyperkalemia, hyponatremia, hypochloremic acidosis (blocks aldosterone effects on Na/H antport) 51. Amiloride – similar to spironolactone; but directly inhibits Na reabsorption in the collecting tubule, therefore works independent of the presence of aldosterone. Unlike spironolactone, ↑ Ca++ reabsorption and this is used to treat Ca++ based nephrolithiasis (formation of sediment or small stones in the kidneys) 52. Triamterene – similar to amiloride but has shorter half life; metabolized by the liver Calcium Channel Blockers ch. 17, 18 53. Verapamil – Non-dihydropyridine Ca++ channel blocker (CCB) that binds Ltype Ca++ channels (long-lasting, voltage dependant, high conductance channels)  inhibits inward movement of Ca++ and ↓ recovery rate of these channels. a. Binds to both types of L-type Ca++ channels  induces ↓ HR and ↓ inotropy, coronary vasodilation, mild peripheral arterial vasodilation b. Clinical: HTN i. SVT: terminates PSVT; rate control of AF and AFL 11

ii. Ischemic heart disease: ↓ HR (↓ myocardial demand) +/- coronary vasodilation (↑ myocardial O2 supply)  ↓ angina iii. Hypertrophic cardiomyopathy: ↓ outflow tract obstruction c. Side effects: Heart block; bradycardia, CHF, edema d. Metabolism: PO for angina and HTN; IV for arrhythmias; hepatic metabolism 54. Diltiazem – a CCB that is similar to verapamil but causes less coronary vasodilation and less negative inotropy 55. Nifedipine – dihydropyridine CCB  inhibits inward movement of Ca++. Acts predominantly on vascular smooth muscle  peripheral arterial vasodilation  triggers compensatory reflex tachycardia. PO, hepatic metabolism a. Clinical: HTN. Primary pulmonary hypertension, Raynaud’s phenomenon, ischemic heard disease b. Side effects: hypotension, CHF, flushing, headaches, dizziness, peripheral edema ACE Inhibitors ch. 16 56. Captopril – Reversibly inhibits angiotensin-converting enzyme (ACE), which catalyzes angiotensin I (ATI)  ATII, thus blocking the RAA axis. The net effect of ACE inhibition is arterial and venous vasodilation and natriuresis. PO, must be taking 3x/day. a. Clinical: HTN. CHF: ↓ afterload, ↓ adverse LV modeling. Reduces proteinuria and progression of nephropathy in diabetes. Ischemic heart disease: ↓ mortality, MI, and need for revascularization. Contraindicated in renal insufficiency, pregnancy, bilateral renal artery stenosis b. Side effects: Hypotension, especially in Na-depleted patients. Angioedema, acute renal failure 57. Enalapril (pro drug) –oral and parenteral angiotensin-converting enzyme (ACE) inhibitor. Drug competes with angiotensin I  inhibiting conversion to angiotensin II (a potent vasoconstrictor and a negative feedback mediator for renin activity)  ↓ angiotensin II plasma levels  ↓ BP and ↑ plasma renin activity a. Clinical: treatment of hypertension and congestive heart failure. It has become a first-line agent for treating heart failure due to its proven reduction of mortality 58. enalaprilat (active form) Drugs for Chronic Heart Failure ch. 16, 17 Cardiac Glycosides 59. Digoxin – Inhibits Na/K ATPase pump, causing ↑ intracellular Na  impairs Na/Ca exchanger  results in ↑ intracellular Ca++. The ↑ Ca++ leads to ↑ stores of Ca++ in the sarcoplasmic reticulum, enabling subsequent AP’s to liberate more Ca++  activates contractile apparatus  positive inotropy. Affects cardiac electrical function: potentates vagal slowing of impulse conduction through the AV node  ↑ AV block a. Clinical: CHF (↑ contractility  shifts ventricular performance curve of the failing heart upward). AF & AFL: control (slow) ventricular rate by ↓ conduction velocity and ↑ refractory period at the AV node. 12

b. Side effects: atrial tachycardia and AV block. Dig delirium (N/V, blurred vision, visual hallucinations) 60. Digitoxin - cardiac glycoside; inhibits cellular Na+/K+ pump (see digoxin) a. Clinical: compared to digoxin, has slower onset, longer half life, larger volume of distribution 61. Strophanthin-g – cardiac glycoside consisting of a molecule of rhamnose linked to a steroid nucleus. An orally administrable medication for treating angina pectoris, heart collapse, hypertonicity, and arrhythmia. Other Cardiotonic Agents 62. Dobutamine – #27 63. Amirinone – a phosphodiesterase inhibitor that ↑ intracellular concentration of cAMP by inhibiting cAMP hydrolysis  prolongs action of protein kinase  ↑ intracellular Ca++  ↑ cardiac contractility (inotropy) a. Side effects: long-term use associated with increased mortality 64. Epinephrine - #35 Beta Blockers 65. Propranolol – #31 66. Sotalol – class III antiarrhythmic with B-blocker ability. Drug blocks rapid outward K current  prolongs repolarization and duration of the AP a. Clinical: used for long-term therapy to ↓ the rate of sudden death following MI. Also very effective in preventing recurrence of arrhythmia and ↓ mortality b. Side effects: ↑ QT interval  syndrome of torsade de pointes (rare, 3-4%) ACE Inhibitors 67. Enalaprilat - #58 Antiarrhythmic Drugs Class I (Na+ Channel Blockers) 68. Quinidine – Class IA antiarrhythmic: moderate Na+ channel blockade. PO, hepatic metabolism a. Purkinje cells: moderate Na-channel blockade  depressing phase 0 depolarization b. Pacemaker cells: ↓ slope of phase 4, ↑ threshold for depolarization c. Selectively blocks frequently used channels (i.e. use dependence) d. Drug has anticholinergic and α -adrenergic blocking effects e. Clinical: Supraventricular arrhythmias: AF, AFL, PSVT f. Side effects: ↑ QT interval and potentially proarrhythmic (torsades de pointes). i. Anticholinergic effect  ↑ AV conduction  ↑ ventricular rate in the setting AF or AFL. α-adrenergic blocking effect  vasodilation and hypotension ii. GI upset. Cinchonism (vertigo, tinnitus, headache) iii. Coomb’s positive hemolytic anemias: quinidine-ab complexes bind RBC’s  RBC destruction 69. Procainamide – similar to Quinidine. Manifests less anticholinergic and αadrenergic blocking effects. 13

a. Side effects: lupus-like syndrome (e.g., arthritis, pleurisy, pericarditis) without vasculitis. 70. Lidocaine – a class IB drug. A local anesthetic; shortens phase 3 repolarization and ↓ duration of the AP. Suppresses arrhythmias caused by abnormal automaticity, unlike Quinidine (suppresses arrhythmias caused by increased normal automaticity). a. Clinical: treating ventricular arrhythmias arising during MI. Has little effect on AV junction arrhythmias (because drug doesn’t markedly slow conduction) b. Side effects: cardiac arrhythmias (huh? Doesn’t it cure that?) CNS effects (confusion, drowsiness, slurred speech, paresthesia, convulsions…sounds like a Saturday night to me) 71. Phenytoin – Inhibits generation of high frequency repetitive AP’s via binding to voltage-sensitive Na+ channels of neurons. Preferentially binds to Na+ channels in the inactivated state and prolongs their refractory period  drug inhibits spread of epileptiform discharges without interfering with normal neuronal depolarizations. PO a. Clinical: DOC for generalized tonic-clonic (grand mal) seizures, also used in partial seizures. Treatment of status epilepticus after initial management with benzodiazepines. Digitalis-induced ventricular arrhythmias. b. Side Effects: Toxicity – nystagmus, diplopia, ataxia, sedation. Gingival hyperplasia and hirsutism with long-term use. Teratogenic Class II (Beta Blockers) 72. propranolol - #31 73. sotalol - #66 74. Esmolol – similar to Metoprolol. Very short half life (10 min) due to metabolism of ester linkage. Only given IV during surgery or diagnostic procedure 75. Acebutolol – similar to Metoprolol. A B1-blocker with intrinsic sympathomimetic activity Class III (AP Prolongation) 76. Amiodarone – Primarily a Class III antiarrhythmic; vasodilator; negative inotropic agent. IV and PO. This drug spans the antiarrhythmic classification schema, its actions fall into each of the four classes: a. Class III: K channel blocker (prolongs repolarization) b. Class I: blocks Na channels c. Class II: B-blocker d. Class IV: Ca++ Channel blocker e. Clinical: Ventricular Arrhythmias: DOC for VT/VF during cardiac arrest. Atrial fibrillation: best drug for maintaining sinus rhythm in patients with paroxysmal AF f. Side effects: ↑ QT interval (doesn’t cause torsade de pointes), thyroid dysfunction, ↑ serum transaminases, pulmonary fibrosis, cutaneous photosensitivity. Microcrystalline deposits in cornea and skin, giving patients a slate grey appearance


77. Bretylium - A parenteral Class III antiarrhythmic agent. Bretylium was originally investigated for use as an antihypertensive. Drug has sympatholytic activity that can induce postural hypotension. Initially, bretylium releases norepinephrine from the
sympathetic ganglia and postganglionic adrenergic nerve terminals. The drug then blocks norepinephrine reuptake, thereby depressing the excitability of the sympathetic nerve terminal. It does not deplete catecholamines or interfere with pre- or postsynaptic conductance. Bretylium also seems to display some vasodilatory activity as well as cardio-stimulatory effects.

a. Clinical: This drug is discontinued in the US. Treatment of ventricular fibrillation and unstable ventricular tachycardia, although it is not considered a first-line agent. Class IV (Calcium Channel Blockers) 78. verapamil - #53 Other Agents 79. digoxin - #59 Antianginal Drugs NO Precursors 80. Nitroglycerin – stimulates guanylate cyclase via NO  ↑ cGMP  ↓ intracellular Ca++ and activation of MLC phosphatase; results in MLC dephosphorylation. Net effect is relaxation of veins and ↑ venous capacitance. NO can cause dilation in both arteries and veins but dosing of nitroglycerin is such that venous effects predominate. a. Clinical: treatment of angina, CHF, controls HTN b. Side effects: hypotension, tachycardia, throbbing headaches (from meningeal artery dilation) 81. isosorbide dinitrate – long acting oral form of nitroglycerin Beta Blockers 82. propranolol - #31 Calcium Channel Blockers 83. nifedipine - #55 Antithrombotic Agents 84. Heparin – IV, SC half-life = 60-90min. A fast acting anticoagulant and naturally occurring glycosaminoglycan with a high binding affinity for antithrombin III (ATIII). ATIII is a serine protease inhibitor that inactivates thrombin and other serine proteases (i.e. factors X, IX, XI). When bound to heparin, ATIII undergoes a conformational change that makes its serine protease binding site more accessible a. Clinical: Prophylaxis and treatment of venous thrombosis and pulmonary embolism. Also used for unstable angina, MO, stroke. Contraindicated in bleeding disorders and active bleeding. Contraindicated in pregnancy and bleeding disorders b. Side effects: Bleeding. Thrombocytopenia 85. Warfarin – an oral anticoagulant that interferes with normal synthesis of vitamin K-dependent clotting factors in the liver. It inhibits the enzyme epoxide reductase 15

 prevents vit. K from being converted to its active form  induces vit. K deficiency. a. Clotting factors II, VII, IX, X, and proteins C and S all require an extra carboxyl group to be added to certain glutamate residues for more efficient interaction with Ca++. Vit K is a necessary cofactor of this carboxylation reaction. b. Effect followed clinically by measuring protime (PT); should rise within 12 hours (factor VII, 2 half-lives), but may take 120 hours (factor II, 2 half-lives) c. Clinical: Prophylaxis and treatment of venous thrombosis and pulmonary embolism. AF, dilated cardiomyopathy, LV aneurysm, prevents thrombus formation in patients with mechanical heart valves d. Side effects: Bleeding (reversible with fresh frozen plasma) 86. Aminocaproic Acid – lysine analog that binds to plasminogen. Normally fibrin can accelerate fibrinolysis by binding to and bringing together plasminogen and endogenous tissue plasminogen activator (tPA). Aminocaproic acid blocks fibrin from binding to plasminogen and thereby inhibits fibrinolysis. PO, IV a. Clinical: reduce hemorrhage due to hypofibrinogenemia, especially during surgery and fibrinolytic therapy. Contraindicated in DIC, hematuria b. Side effects: thrombi formed during treatment don’t lyse (could lead to renal obstruction). Hypotension 87. Dipyridamole – PO. Inhibits platelet activate by ↑ platelet cAMP levels via two mechanisms a. blocks uptake of adenosine  stimulation of adenyl cyclase to ↑ production of cAMP b. Inhibits phosphodiesterase: ↓ degradation of cAMP c. ↑ cAMP  ↓ vascular tone (vasodilation)  in normal vessels can take blood from maximally dilated stenotic vessels (shunts blood away from stenotic vessels) d. Clinical: prophylaxis of thromboembolic events in patients with Hx of TIA or CVA. Used to perform pharmacologic cardiac stress test e. Side effects: headache, diarrhea 88. Vitamin K (phytonadione) – stops bleeding problems due to oral anticoagulants. Response to vitamin K is slow (~24h), if immediate hemostasis is necessary  fresh frozen plasma 89. Streptokinase – IV infusion. First-generation non-fibrin-selective fibrinolytic produced by beta-hemolytic strep. SK posses no intrinsic enzymatic activity  doesn’t directly convert plasmin to plasminogen. SK combines with plasminogen  conformational change on the plasminogen exposes active site  SKplasminogen and SK-plasmin complexes convert free plasminogen to plasmin a. Clinical: thrombolysis to treat acute MI. contraindicated in any bleeding problems (intracranial bleed, CVA, intracranial neoplasm, AVM, etc) b. Side effects: Bleeding. Allergic reaction can arise from prior strep infections or prior administration of SK


90. Urokinase – similar to streptokinase. A two-chain serine protease generated by the kidney. Directly converts plasminogen to plasmin  preventing formation of ureteral blood clots. Non-fibrin selective 91. Tissue Plasminogen Activator (t-PA, alteplase) – rapidly activates plasminogen that is bound to fibrin in a thrombus (fibrin selective); lyses only the fibrin. a. Clinical: MI, massive PE, acute ischemic stroke (TIA). Superior to streptokinase in dissolving older clots. b. Side effects: GI Bleeds, cerebral bleeds 92. acetylsalicylic acid (aspirin) – Irreversibly inhibits cyclooxygenase COX 1 and COX 2, blocking arachidonic acid and blocking production of prostaglandins a. Anti-inflammatory: Inhibits migration of WBC’s, stabilizes lysosomes b. Antipyretic: interferes with PGE2 synthesis (PGE mediates resetting body’s thermostat in response to IL-1 in the hypothalamus) c. Antiplatelet: ↓ platelet production of TXA2 (platelet activator, vasoconstrictor); ↓ PGI2 (platelet aggregation inhib. & vasoconstrictor) d. Clinical: Analgesia and inflammation: headaches, arthritis, dysmenorrhea, myalgias. Acute therapy for MI, unstable angina, and TIA. Prophylaxis against MI and CVA. Antipyretic (reduces or prevents fever) i. Contraindicated in hemophilia, peptic ulcer disease patients, children with viral syndrome (Reye’s syndrome) e. Side effects: gastritis, GI bleeding, renal failure Antiatherosclerotic Agents 93. Cholestyramine – Medium reductions in total cholesterol and LDL, small ↑ in HDL, small ↑ in triglycerides. Large, nonabsorbable polymer that binds bile acids in the intestine  interrupts enterohepatic bile acid circulation. The ↑ excretion of bile acids  ↑ conversion of cholesterol to bile acids in liver  results in up-regulation of hepatic LDL receptors  ↑ clearance of LDL from plasma. a. Clinical: second-line drug for hypercholesterolemia b. Side effects: bloating, indigestion, N/V, constipation. In high doses: steatorrhea, deficiency of lipid soluble vitamins (A,D,E,K) c. Contraindicated: hypertriglyceridemia 94. Niacin (nicotinic acid, vit. B3) – Large reduction in TAG, medium ↑ in HDL, medium ↓ in total cholesterol and LDL. Inhibits hepatic synthesis and secretion of VLDL  ↓ substrate for endogenous LDL production. ↑ peripheral lipoprotein lipase activity  improved VLDL clearance and ↓ TAG. ↓ catabolism of HDL. a. Clinical: hypercholesteremia, low HDL b. Side effects: flushing, pruritus, GI distress, glucose intolerance, ↑ transaminases, hyperuricemia, gout 95. Gemfibrozil – Large reduction in TAG, medium ↑ in HDL, medium ↓ in total cholesterol and LDL. Drug is a fibric acid derivative that reduces plasma TAG by ↓ VLDL by three mechanisms: a. ↑ activity of lipoprotein lipase  promote catabolism of VLDV


b. ↓ hepatic synthesis and secretion of VLDL c. ↑ HDL (↓ TAG  ↓ exchange of cholesteryl esters from HDL to TAGrich lipoproteins) d. Clinical: hypertriglyceridemia, low HDL e. Side effects: GI distress, rash, myopathy, gallstones 96. Clofibrate – similar to gemfibrozil. A fibric acid derivative that is less well tolerated. 97. Lovastatin – Inhibits HMG CoA reductase  inhibits de novo synthesis of cholesterol  depletes supply of cholesterol. Also increases LDL receptors  ↓ in plasma cholesterol a. Clinical use: lowers plasma cholesterol in all types of hyperlipidemias b. Side effects: liver function problems, myopathy and rhabdomyolysis (disintegration of muscle) 98. Probucol - Inhibits the transport of cholesterol from the intestine and may interfere with the conversion of acetate to mevalonic acid, an early stage in cholesterol synthesis. It is known not to affect the later stages of cholesterol synthesis. PO a. Clinical: Oral antilipemic agent used in the treatment of primary hypercholesterolemia. b. Side effects: abdominal pain, dizziness, angina, diarrhea Antianemic Drugs 99. ferrous sulfate (Iron) – corrects deficiency of ferritin due to chronic blood loss or insufficient intake 100. Deferoxamine - an iron-chelating agent used in the treatment of acute iron intoxication and chronic iron overload. Ferric ions bind to the 3 hydroxamic groups of
deferoxamine, creating ferrioxamine, a stable, water-soluble complex that is then readily excreted by the kidneys. Drug affinity for iron is greater than that of other chelating agents, and administration of the drug does not appear to increase the excretion of electrolytes or other trace minerals

101. cyanocobalamin (vitamin B12) – deficiency can result from either low dietary levels or poor absorption due to ↓ intrinsic factor in the parietal cells a. Clinical: folic acid masks B12 deficiency  treat megaloblastic anemia with both B12 and folic acid 102. folic acid – deficiency caused by increased demand (lactation), poor absorption, alcoholism, treatment with dihydrofolate reductase inhibitors (methotrexate and trimethoprim) a. Clinical: deficiency  megaloblastic anemia from ↓ synthesis of purines and pyrimidines  inability of erythropoietic tissues to proliferate Anti-hypertensive Drugs Diuretics 103. hydrochlorothiazide - #46 104. furosemide - #47 105. ethacrynic acid - #48 106. torsemide - #49 107. triamterene - #52 108. spironolactone - #50 109. amiloride - #51 18

Vasodilators 110. Hydralazine – Activates guanylate cyclase  ↑ cGPM  dephosphorylation of myosin  smooth muscle relaxation and ↑ permeability to K+ (hyperpolarization). Net effect is arterial vasodilation a. Clinical: HTN; not a first line antihypertensive but useful as an additional agent in patients with refractory HTN. Relatively rapid onset of action and IV availability contribute to its utility in hypertensive emergencies. i. CHF; ↓ afterload (also given with nitrates to ↓ preload as well) b. Side effects: Headache, N/V, flushing. i. Self-limited lupus-like syndrome (~10%) ii. Reflex ↑ HR, contractility, renin activity, and fluid retention in response to vasodilation. 111. Minoxidil – similar to hydralazine. IV, onset after 30 seconds, lasts 2-3 min. More potent agent best known for its side effect, hypertrichosis (excessive hair growth in non-androgen-sensitive areas of the face) 112. Nitroprusside – contact with RBC’s leads to decomposition of the drug and release of NO. NO, via activation of guanylate cyclase,  vasodilation in both arteries and veins  ↓ preload and afterload a. Clinical: Hypertensive crisis i. Acute aortic dissection. Must be given concomitantly with a Betablocker to prevent reflex tachycardia and ↑ contractility, both of which would lead to an increased rate of pressure development  further progression of the dissection ii. Refractory CHF b. Side effects: Hypotension, reflex tachycardia. Cyanide toxicity: inhibition of cellular respiration  lactic acidosis, arrhythmias, hypotension, cytotoxic hypoxia. Thiocyanate toxicity: weakness, disorientation, psychosis, muscle spasm Adrenergic Receptor Blockade 113. propranolol - #31 114. prazosin – #25 115. metoprolol - #33 116. Pindolol – similar to Propranolol (#31). A B-blocker with intrinsic sympathomimetic activity (i.e. a partial B-agonist), making it relatively unlikely to cause bradycardia 117. timolol - #34 Neuronal Blockade 118. guanethidine - #43 Neurotransmitter Depletion 119. reserpine - #41 Central Nervous System 120. clonidine - #21 121. α-methyldopa - #42 122. reserpine - #41 Calcium Channel Blockers 123. nifedipine - #55


ACE Inhibitors 124. captopril - #56 125. enalapril (pro drug) - #57 126. enalaprilat (active form) - #58 Angiotensin II Receptor Antagonists 127. Losartan – angiotensin-receptor blocker (ARB). Potent antagonist of the angiotensin type 1 receptor a. Clinical: HTN, can be used as an ACE inhibitor substitute in patients who cannot tolerate ACE inhibitors b. Side effects: similar to other ACE inhibitors. Don’t produce cough


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