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Old 07-06-2012
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Drug Autonomic Pharmacology Concept!

I have a question regarding autonomic pharmacology.
I have often seen the receptor/neurotransmitter distribution for Sympathetic, parasympathetic and skeletal muscle. Based on what i have seen, I am assuming that either Acetylcholine or nicotine can stimulate the Nn receptors located at the ganglions for both sympathetic and parasympathetic, leading to further neurotransmitter release at level of effector organ.

However, why does this not make nicotine/Varenicline, a ganglionic agonist that stimulates BOTH symp./parasymp.?

So, why do not organophosphates, (that I assume, simply prolong ACh effect duration), also cause activation of BOTH symp./parasymp., since they are basically raising active Ach levels, irrespective of location?

Yet, organophosphate poisoning produces effects typical of Parasymp. agonism. Why is this occuring and not the dual activation of both autonomic nervous system arms cancelling each other out?
Is this due to some kind of predominance or that drugs are peripheral action only? (because the diagrams list ganglia for both symp./parasymp. outside the vertebral canal)

Even then, why does not the prolonged Ach not affect the exclusively symp. controlled actions like ionotropy for heart? (as I have never read Positive ionotropy as a side effect of organophosphate poisoning).

I know I have asked a considerable number of questions but I would greatly appreciate an early response as my preparation has been halted specifically due to this question.
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