PHARMACOLOGY OF AUTONOMIC NERVOUS SYSTEM. ALL YOU NEED TO KNOW FROM SNELL NEUROANATOMY.

 

·      Ganglion stimulating agents: bind with nicotinic receptors on post synapting membrane initiating fast EPSP to cause sympathetic or parasympathetic response. Eg: nicotine, lobeline and dimethyl-pipera-zinium.

·      Ganglion inhibiting agents: hexa-methonium and tetra-ethyl-ammonium bind with nicotinic receptors and do not let ACH bind with it. Nicotine in high concentrations bind with nicotinic receptors causing depolarization and maintaining it (depolarization is not followed by repolarization and action potential is not generated). Muscurinic receptors on post synaptic membrane can be blocked by atropine.

·       Stimulation at neuroeffector junction: PHENY-EPHIRINE: alpha receptor stimulator. ALBUTEROL & METAPROTERENOL: beta 2 receptor stimulator causing bonchodilation.

·      Inhibition at neuroeffector junction: alpha receptors can be blocked by phenoxybenzamine while beta receptors can be blocked by propranolol. Reserpin is a drug that does not allow synthesis of norepinephrine inside the postganglionic axon and thus it is not released in the neuroeffector synaptic cleft. {acetylcholine is formed from dopamine inside the postganglionic axon, but dopamine before converting into ACH has to be preserved in a vesicle or else it would be destroyed by monoamine-oxidase (MAO), an enzyme present freely in the cytoplasm of the axon. Reserpin binds with the vesicle and does not allow dopamine uptake and dopamine is destroyed by MAO}. Muscurinic receptors on target organs can be blocked by atropine.