| A | B |
| Cranio-Sacral outflow | Parasympathetic Nervous System |
| Thoraco-Lumbar outflow | Sympathetic Nervous System |
| Ganglion | Collection of nerve cell bodies outside the CNS |
| Nuclei | Collection of nerve cell bodies within the CNS |
| Pre-ganglionic parasympathetic nerve fibers | cholinergic fibers |
| Pre-ganglionic sympathetic nerve fibers | cholinergic fibers |
| Post-ganglionic parasympathetic nerve fibers | cholinergic fibers |
| Post-ganglionic sympathetic nervefibers | adrenergic fibers (mostly) |
| sweat secretion | stimulated by sympathetic CHOLINERGIC fibers |
| SA node | predominantly controlled by Vagus n.(cholinergic) |
| peripheral vascular smooth muscle | contracted by sympathetic (adrenergic) fibers |
| bronchial smooth muscles | constrict upon parasympathetic (cholinergic) stimulation |
| bronchial smooth muscles | dilate upon sympathetic (adrenergic) stimulation |
| atropine | competitive blocker at mAChR |
| curarine | competitive blocker at nAChR |
| mACh receptors | found at cholinergic synapses of smooth muscles |
| mACh receptors | found at cholinergic synapses of exocrine glands |
| mAChR | stimulation will increase (exocrine) glandular secretions |
| mAChR | blockade will decrease (exocrine) glandular secretions |
| nACh receptors | found at neuro-muscular junction (NMJ) |
| Meuro-muscularJunction (NMJ) | a cholinergic synapse |
| nAChR | found in the end-plate region of skeletal muscles |
| nAChR stimulation | will increase skeletal muscle tone |
| overstimulation of nAChR | can cause 'muscle spasms' |
| nicotine | stimulates AChR at NMJ and in autonomic ganglia |
| muscarine | stimulates mAChR in smooth muscles and exocrine glands |
| alpha-adrenergic receptors | predominate in the peripheral vascular smooth muscle |
| alpha-adrenergic receptor stimulation | will cause vasoconstriction and increase BP |
| beta-adrenergic receptor stimulation | will cause vasodilation in peripheral vasculature |
| beta-adrenergic receptor stimulation | will result in positive ino-tropic effect on myocardium |
| alpha-adrenergic receptor stimulation | in SA node will cause positive chrono-tropic effect on heart |
| beta-adrenergic receptor blockers | will decrease myocardial force of contraction and reduce cardiac output |
| alpha-adrenergic receptor blockers | will prevent sympathetic vasoconstriction and reduce BP |
| beta-adnergic receptor stimulation | will cause broncho-constriction |
| ACh Esterase (AChE) | foundin ALL cholinergic synapses |
| AChE | hydrolyzes the ester bond in acetylcholine |
| AChE inhibition | will increase synaptic transmission at ALL cholinergic synapses |
| AChE inhibitors | will cause salivation, lacrimation, urination, and defecation |
| sphincter muscles of iris | constricted by parasympathetic stimulation |
| radial muscles of iris | contracted by sympathetic stimulation |
| effects of acetylcholine binding Nicotonic receptor | Increased Na+ influx/K+ efflux |
| effects of acetylcholine binding @ Muscarinic receptor | Increase IP3/DAG |
| Increase IP3/DAG | Result of EPI/NE binding @ α-1 receptor |
| Iris radial mm., skin splanchnic vessels | location of α-1 receptors |
| Result of EPI/NE binding @ α-2 receptor | Decrease cAMP |
| α-2 receptor location | Presynaptically on sympathetic terminals, skin splanchnic vessels smooth mm |
| Result of EPI/NE binding @ β-2 receptor | Increase cAMP |
| Result of EPI/NE binding @ β-1 receptor | Increase cAMP |
| β-2 receptor location | bronchial smooth mm., skeletal mm. |
| β-1 receptor location | heart |
| Muscarinic Cholinergic Receptor Agonists | Muscarine, Bethanecol, Pilocarpine |
| Physostigmine | Forms covalent bond with AchE that is resistant to hydrolysis |
| Edrophonium | Forms an electrostatic/H-bond that is reversible; Short-lived inhibition |
| Phosphorylates the active site of AchE and forms a bond that is extremely stable | Malathion, echothiophate |
| can undergo aging where there is strengthening of the AchE-phosphorus bond | Malathion, echothiophate |
| Strong nucleophile that can break the AchE-phosphorus bond, as long as aging has not occurred | Pralidoxime |
| Used for organophosphate intoxication | Pralidoxime |
| Atropine-Organ effects | Eye: dilation |
| Atropine-Organ effects | Heart: tachycardia due to blockade of vagal slowing |
| Atropine-Organ effects | Respiratory: bronchodilation |
| Atropine-Organ effects | GI: dry mouth, reduced motility |
| Mecamylamine | Block nicotinic receptors present on post-ganglionic neurons of both the sympathetic and parasympathetic NS |
| Mecamylamine-Organ system effects | Eye: loss of accommodation |
| Mecamylamine-Organ system effects | Heart: hypotension |
| Mecamylamine-Organ system effects | GI: reduced motility |
| adrenergic receptors are located mainly on vascular smooth mm | they mediate arteriolar and venous tone |
| activation of ? leads to an increase in peripheral vascular resistance and BP and usually a decrease in HR due to the vagal reflex | α-adrenergic receptors |
| clonidine | α-2 adrenergic receptor agonist |
| α-adrenergic receptor agonists | direct sympathomimetics |
| β-adrenergic receptor agonists | direct sympathomimetics |
| Phenylephrine | α-1adrenergic receptor agonist |
| β1/β2-agonists | isoproterenol, ephedrine, pseudoephedrine |
| β2-agonist | tertbutaline |
| decrease BP while increasing HR and force of contraction | β-agonists will |
| Cocaine | Inhibits reuptake at noradrenergic synapses |
| Amphetamine | Increases release of catecholamines |
| Tyramine | Increases release of catecholamines |
| Organ system effects: indirect sympathomimetics | Blood vessels: constriction mediated mainly by α-1 receptors |
| Organ system effects: indirect sympathomimetics | Heart: increased contractility and HR mediated by β1 |
| Organ system effects: indirect sympathomimetics | BP: increases |
| Organ system effects: indirect sympathomimetics | Eye: mydriasis mediated by α-receptors |
| Organ system effects: indirect sympathomimetics | Respiratory tract: relaxation mediated by β2 receptors |
| α1>>>>α2 | prazosin |
| α1>α2 | phenoxybenzamine |
| α1=α2 | phentolamine |
| yohimbine | α2 |
| Organ system effects α-adrenergic receptor antagonists | Lower peripheral vascular resistance and BP |
| (lol!) | β-adrenergic receptor antagonists |
| β-adrenergic receptor antagonists | these compounds block both β1 and β2 receptors |
| Organ system effects: β-adrenergic antagonists | Heart: reduce BP |
| Organ system effects: β-adrenergic antagonists | Respiratory: can cause increased airway resistance when β2 receptors are blocked |
| Organ system effects: β-adrenergic antagonists | Eye: reduces intraocular pressure |
| Reserpine | Inhibits VMAT, resulting in depletion of catecholamine stores |
| Metyrosine | Blocks tyrosine hydroxylase and reduces catecholamine synthesis |
| Sympatholytics | Reserpine, Metyrosine |