Name Effect Duration Therapeutic use Adverse effects

Phenoxybenzamine -Abilty to block presyn. Inh. A2 rec. in 24h, body -Pheochromocytoma -Post. Hypot.
heart hast to synth. -Prior to tumor removal to prevent hypot. Crisis -Nasal stuffiness
(noncomp., irrev.) -> more epin. Release New -Sometimes at Raynaud disease -Nausea, vomiting
->B1 rec. in heart stim.-> more co receptors -May inhibit ejaculation
-Reflex tachycardia
-Epinephrine reversal
Phentolamine -Post. Hypot. 4h -Short term management of pheochromocytoma -Can trigger arrhythmias (contraind. in
-Epineph. Reversal -In hyperten. Crisis due to abrupt withdrawal of patients with coronary art. Disease)
(comp., -Reflex tachycardia clonidine and from ingesting tyramine-containing
foods in patients taking monoamine oxidase inhibitors
Prazosin, Terazosin, -Useful in treatment of hyperten. (relax. Doxa. Longest -Tam. Least effect on BP (more selective for A1a in -Minimal changes in co
Art. And ven. Sm.msc.) acting prostate and bladder) -Dizziness, drowsiness, lack of energy
Doxazosin, Tamsulosin, -Tam. And Alfu. Good for BPH -First dose only 1/3 or ¼ to prevent syncope -Retrograde ejaculation
Alfuzosin -Modest improvement in lipid and glucose met. -Floppy iris syndrome
(sel. A1) -Never used as monotherapy (inferior cv outcomes)
-BPH
Yohimbine -Works at level of CNS-> increase of -contraindicated in cardiovascular disease,
symp. Outflow to periphery psychiatric conditions, and renal
(sel., comp. A2) dysfunction because it may worsen these
conditions

Name Effect Therapeutic use Adverse effect

Propranolol -Decreased symp. Outflow from CNS -Hypertension (does not reduce BP in patients with normal values) -Bronchoconstriction (exacerbation of COPD or Asthm)
(nonselective) -Neg. inotropic and chronotropic effect on heart-> lower co-> lower -Chronic management of stable angina -Lower glycogenolysis and glucagon release-> hypoglycemia
O2 consump. -Prophylaxis for second MI or reduction of size in acute MI -Can prevent counter regulatory effects in hypoglycemia
-Depresses SA and AV node -effective in attenuating supraventricular cardiac arrhythmias, but -blocked action of isoproterenol (B1,2 agonist)->A receptor action
-During stress/effort attenuated HR generally are not effective against ventricular arrhythmias (except still going
-B2 block + reflex peripheral constriction due to low CO-> those induced by exercise) -cardiac arrhythmias when stopped abruptly (<few weaks)
vasoconstr. In muscles (normalized BP values on long term) -migraine prophylactically-> due to its lipophilic nature -upregulation of B receptors-> can worsen angina or HT on
-Inhibition of renin release -blunting symp. Stimulation in hyperthyroidism suspension of therapy
-reduced activity of B2,3 receptors->lower lipase activity-> high LDL,
TG low HDL
-depression, dizziness, fatigue, visual disturbances
Nadolol, Timolol -more potent than Propranolol Topically applied against chronic open angle glaucoma (effect lasts
(nonselective) -Timolol decreases secretion of aqueous humor by ciliary body 12-24h)
Acebutolol, Atenolol, Bataxolol, Bisoprolol, Esmolol, Metoprolol, Cardioselective Acebutolol, Atenolol, Metaprolol -Hypertensive patients with pulmonary disorder
Nebivolol Antagonize B2 only at very high doses (50-100x the B1 dose) First-line therapy drugs for chronic stable angina
(sel. B1) -Minimized bronchoconstrictive effect, peripheral resistance and -Bisoprolol and extended release formulation of Metoprolol are
carb. Metabolism disturbance indicated in chronic heart failure
-Lower BP in HT, increase exercise tolerance in angina
-Esmolol short half life-> only available iv-> used to control BP and
heart rhythm during
-Nebivolol releases nitric oxide from endothelial cells-> additional
vasodilation
Acebutolol, Pindolol -not pure antagonists -β-blockers with ISA are effective in hypertensive patients with
(Antagonists with partial Agonist activity) -Also have the ability to weakly stimulate both β1 and β2 receptors moderate bradycardia
-Have intrinsic sympathomimetic activity (ISA) -Not used for stable angina or arrhythmias due to their partial
-Stimulate the β receptor to which they are bound + inhibit agonist effect
stimulation by more potent endogenous catecholamines
(epinephrine and norepinephrine)
-minimize the disturbances of lipid and carbohydrate metabolism
that are seen with other β-blockers
Labetalol, Carvediol -Nonselective B and A1 blocking actions-> peripheral vasodilation -Labetalol-> pregnancy induced HT -Orthostatic hypotension-> A1
(A&B Antagonist) (other B blockers produce initial vasoconstriction) -Carvediol-> stable chronic heart failure -Dizziness-> A1
Carvedilol also decreases lipid peroxidation and vascular wall
thickening-> good for heart failure
Reserpine Blocks the Mg2+/adenosine triphosphate– dependent transport of -Slow onset
biogenic amines (norepinephrine, dopamine, and serotonin) from -Long duration of action
the cytoplasm into storage vesicles in the adrenergic nerve terminals -Effects persist for many days after discontinuation
in all body tissues -Has been used for the management of hypertension but has largely
Ultimate depletion of biogenic amines been replaced with newer agents with better side effect profiles and
-Decreased release of norepinephrine fewer drug interactions
->Impaired Sympathetic function