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hypotension o Angina o Cardiac arrhythmias o ADHD o Asthma o Glaucoma and other eye diseases o Allergies (usually life threatening) o Urinary retention (bladder atony) vs. incontinence o Hyperthyroidism o Immunological diseases o BPH o Pesticides and Nerve gases (will just be mentioned, most exert toxicities through ANS) Organization of the ANS o Receptors ---(Afferent) Brain and spinal cord –(Efferent)-SNS and PNS Receptors: no drugs act CNS: some drugs act Efferent: MOST drugs act! o Anatomy: Most tissues have input from both SNS and PSNresult is from “net tone” SNS: acts as 1 unit (speed up HRincreases SNS tone everwhere) vs. PNS: can act discretely All of Epi comes from adrenal glands Epi in CNS stays there and Epi made peripherally stays there o Two neuron chain:
but in reality. transmitter release is en passant. 70-75% normally)] SNS: o α1: constriction of vascular SM (usually predominatesincrease TPRincrease DBP o β2: relaxation of vascular SM PNS: muscarinic (no innervation): dilation o We don’t know why R’s are here Lungs: Bronchial SM SNS: β2: relaxation-bronchodilation . we will use classical model for simplicity. Note: For SNS.e. give muscarinic agonist to contract longitudinal muscle But also causes: Radial contractionnear clear. along the length of the axon there are swellings where NE released (not just the terminal bouton)can innervate much larger region of tissue PNS and SNS Physiology in Various Organs: Eye: SNS: Dilator Muscle: α1 receptors PNS: o Constrictor Muscle Dominates slightly over dilator muscle at rest o Ciliary Muscle Radial: Controls lens Relaxation lens tension (>20 feet: far vision) Contractionaccommodation (<20 feet: near vision) Longitudinal: for outflow of aqueous humor Contractionpulls open Canal of Schlemm o Clinical Scenario: For glaucoma (increase in IOP). With lots of vasodilationdecrease in DBP and VRdecrease CO and SBP – more blood in veins [80-85% vs. far blurry Constrictor contractionpoor night vision Heart: Think of as controlling SBP SNS: β1 increase rate and force of contraction o Increase COincrease SBP o Clinical Scenario: β blockers reduce rate and force of contraction and decrease SBP PNS: muscarinicdecrease rate and force of contraction o Decrease COdecrease SBP Blood vessels (arteries and arterioles primarily): Think of peripheral resistance as controlling DBP (Note: Can’t always think of heart and blood vessels separately: Ex. i.
o SNS: suppress digestion/defecation/urination o PNS: promote digestion/peristalsis/defecation/urination Bladder Detrusor Muscle: muscle in wall of bladder o SNS: β2 relaxation o PNS: contraction Internal Sphincter (urethral sphincter): must relax to urinate o SNS: α1 contraction o PNS: relaxation Note: SNS activation tends to increase urge to urinate. but is supposed to suppress urinationwhy? Because increase in COincrease in GFRmore urine Uterus SNS: o α1: increase contraction Clinical: NOT used to induce labor because oxytocin is better inducer o β2: decrease contractions Clinical: used to suppress labor PNS: NONE HERE Salivary Glands SNS: α1. β2: increase viscous secretions o Clinical: Really only seen in life-threatening situations PSN: increase in watery secretions . PNS: muscarinic: bronchoconstriction Clinical Scenario: For asthma. give β2agonsts or muscarinic blockers o NEVER give a β blocker or a muscarinic agonist GI Tract Smooth Muscle o SNS: β2 relaxation o PNS: constriction Sphincters o SNS: α1 contraction o PNS: relaxation In summary.