Pharmacology of Autonomic Agents

Neurotransmission at both cholinergic and adrenergic synapses can be influenced by a variety of naturally occurring and synthetic drugs (Table 38.2). For example, ACh secretion is drastically reduced in the presence of botulinum toxin which contains proteases that cleave proteins vital to the process of exocytosis. Nicotine, one of the active ingredients in tobacco can mimic the effects of ACh and increase (or decrease at high doses) autonomic ganglionic transmission as well as that at the 

NE secretion can be effectively decreased by administration of reseipine, an alkaloid isolated from a small woody perennial found in India (Rauwolfia), which has a high affinity for the vesicular monoamine h ansporter-2 (VMAT-2) and as such prevents NE storage. Alternatively, NE secretion can be increased by administration of tyramine (decarboxylated tyrosine), which is a constituent of a variety of foods including red wine, pickled herring and cheese. Amphetamine has a similar effect, which is most prominently manifested in the CNS. The termination of NE effects can be circumvented by the administration of cocaine, which blocks NE transport into presynaptic nerve endings (NET) an effect, which is also shared by some of the first generation antidepressants, such as imipramine. 

Perhaps the most widely knowm agent to alter cholinergic transmission is the belladonna alkaloid, atropine. This agent is relatively selective for muscarinic receptors and as such decreases exocrine gland secretion, smooth muscle tone and the effects of vagal nerve stimulation of the heart. Atropine has several clinical applications including use as a preoperative medication, post-myocardial infarction to increase heart 

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