Which is correct regarding the parasympathetic branch of the autonomic nervous system quizlet?

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The answer is B. The postganglionic sympathetic fibers innervating sweat glands and arrector pili muscles are cholinergic. That is the exception to the rule that all postganglionic sympathetic fibers are adrenergic. How do you know it's cholinergic? A variety of biochemical and histochemical methods can prove that ACh is the neurotransmitter. They also show that there is abundant acetylcholinesterase (AChE), which hydrolyzes ACh, in the synaptic cleft. But we're going to make the assessment pharmacologically: We can prevent release of neurotransmitter from nerve g with botulinum toxin, which affects only (and all) cholinergic nerves; and we can prevent the response of the sweat glands innervated by nerve g with atropine, the prototype muscarinic receptor antagonist- a drug that has no effects on nicotinic (or other) receptors (eg, answer d) at usual doses. Likewise, nicotinic receptor blockers (or nicotine itself) have no effect at this site-another reason why answer d is incorrect. And how you do know it's part of the SNS? Sweat glands are activated (secretions are increased) and arrestor pili muscles contract (the hair on our skin stands on end) when the entire SNS is activated, such as in the fight or flight response;" and if you trace the origins of the preganglionic nerves that activate the postganglionic ones, they emanate from the same regions of the spinal cord from which all other sympathetic preganglionic fibers arise- the thoracic and lumbar regions. Cocaine (a) is incorrect. It, and tricyclic antidepressants (eg, amitriptyline, imipramine, etc), block neuronal reuptake of NE. That is, its site of action is at the neuroeffector junction of postganglionic sympathetic neurons (nerve d)-all of them except those that innerva te most sweat glandsand arrector pili muscles, of course.

The answer is D. Reserpine blocks intraneuronal synthesis and storage of norepinephrine ( NE ), and the ability of the reuptake process to re-store norepinephrine that has already been released from an activated adrenergic nerve, thereby exposing the free intraneuronal NE to degradation by intraneuronal MAO . This is important for other reasons : the final synthesis of NE from its precursor, dopamine, occurs in the vesicles. If dopamine entry is blocked, as it is by reserpine, NE synthesis is decreased. Reserpine also blocks vesicular uptake of dopamine in parts of the CNS Pargyline (a) is a nonselective MAO inhibitor. Note that unlike reserpine, MAO inhibitors do not inhibit intraneuronal storage of NE. Rather, they inhibit metabolic inactivation of NE in adrenergic nerve endings (or, at other sites, other monoamines). This leads to a "build-up " of norepinephrine in adrenergic nerve endings. Prazosin (b) and propranolol (c) are adrenergic receptor blockers (α₁, and β₂, respectively ) and have no direct effect on NE storage. Tyramine (e) is an indirect-acting sympathomimetic that displaces and releases neuronal NE via a process that does not involve exocytosis.

The answer is B. Cocaine ( and tricyclic antidepressants such as imipramine) are classic examples of drugs that inhibit catecholamine reuptake by the "amine pump, " which is the main process by which released NE ( or dopamine ) re-enters the neuron and its receptor-mediated effects are terminated physiologically In the presence of cocaine or a tricyclic, released neurotransmitter lingers and accumulates in the synapse (neuroeffector junction ), and so pertinent adrenergic responses appear heightened or more intense, and prolonged. The pump is also important for the neuronal uptake , and ultimate effects , of such catecholamine-releasing drugs as ephedrine, pseudo-ephedrine , amphetamines , methylphenidate , and tyramine long as an adrenergic synapse is present (as it is in the diagram ) and exposed to cocaine or a tricyclic antidepressant , the drugs effects are not dependent on whether the effector (target) is smooth muscle, cardiac muscle, or an exocrine gland of any sort. Cocaine has no direct effect on α₂-adrenergic receptors (a), nor on any of the postsynaptic adrenergic receptors (c). Likewise, the drug has no effect on MAO (d) nor on the exocytotic release of NE in response to an action potential (e). There is no direct functional link between the amine pump and such processes as NE release (exocytotically or otherwise ) or activation of presynaptic (α₂) adrenergic receptors.

The answer is E. Prazosin selectively and competitively blocks adrenergic receptors and, unlike many other a-blockers (phentolamine, phenoxybenzamine), has virtually no presynaptic (a) effects at usual doses. None of the other drugs fit the bill: Clonidine (a) is a centrally acting α-adrenergic agonist used mainly as an antihypertensive drug. The main consequence of that effect is a reduction of " sympathetic outflow " that reduces all of the three main determinants of blood pressure: heart rate, stroke volume, and total peripheral resistance Phentolamine is a competitive α-blocker, but it blocks both presynaptic (α₂) and postsynaptic (α₁) receptors more or less equally well. Phenoxybenzamine (c) is similar to phentolamine in terms of its receptor targets. However, phenoxybenzamine actions last far longer than those of phentolamine, and they arise from noncompetitive/reversible α-blockade (Rather than merely occupying the receptors, as is the case with most antagonists, phenoxybenzamine alkylates the receptors, permanently impairing the ability to interact with suitable agonists). Phenylephrine (d) is a strong agonist for all the α-adrenergic receptors, has no α-antagonist activity, and exerts no direct effects of any type on β-receptors.

The answer is A. The description of this drug is, in reality, also an excellent description of many of the properties of atropine, the prototype muscarinic receptor locking drug , and of nearly a dozen other antimuscarinics marketed for "overactive bladder." In terms of bladder function, paras ympa thetic influences tend to promote urine flow; antimuscarinics, then, tend to suppress that effect. (Conversely , sympathetic influences , via α-adrenergic receptor activation, tend to suppress urine flow and α-adrenergic blockers cause the opposite.

Festoterodine is a relatively new drug that was heavily marketed to prescribers and directly to consumers. It is indicated for the treatment of an overactive urinary bladder, reducing the symptoms of urge incontinence, urinary urgency, and urinary frequency. It prevents physiologic activation of the bladder's detrusor and simultaneously prevents relaxation of the sphincter. Side effects include constipation, dry mouth, blurred vision, photophobia, urinary retention, and slight increases in heart rate. Another advisory for the drug: Heat stroke and fever due to decreased sweating in hot temperatures have been reported. Festoterodine has no direct effects on blood vessels that might change blood pressure. Based on this information, what prototype drug is most like festoterodine?

a. Atropine
b. ß-adrenergic blockers (eg, propranolol)
c. Isoproterenol
d. Neostigmine
e. Phentolamine

The answer is D. In "cholinesterase poisoning," we are dealing with overstimulation (from accumulated ACh) of both peripheral muscarinic and nicotinic receptors. Recall that atropine is a specific muscarinic receptor blocker, and the muscarinic receptors are the ones found on such structures as smooth muscle, cardiac nodal tissue, and exocrine glands. In contrast, the cholinergic receptor on skeletal muscle is nicotinic, so skeletal muscle isn't affected by atropine. If one receives a lethal dose of a cholinesterase inhibitor, he or she may be a little more comfortable (less defecation, urination, respiratory tract mucus hypersection and bronchoconstriction, after the atropine is given, but they are still likely to die from skeletal muscle (NM nicotinic) overstimulation and then paralysis. Paralysis of the diaphragm and intercostal muscles are the most lethal consequences.

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