Effects Of Neurotransmitters

The binding of ACh to nicotinic receptors located on postganglionic neurons induces changes in membrane potential called fast excitatory postsynaptic potentials. Fast excitatory postsynaptic potentials, if strong enough and frequent enough, in turn induce action potentials that are transmitted to the synaptic terminals of the postganglionic nerves. These action potentials in turn result in the release of transmitter onto the effector organs.

Terminals of postganglionic fibers of the parasympa-thetic system release ACh, which interacts with muscari-nic receptors located on the effector. It is impossible to assign any general effector response such as excitation or inhibition to this type of cholinergic receptor. Stimulation of muscarinic receptors in the atria of the heart decreases both heart rate and the force of contraction, whereas activation of muscarinic receptors on intestinal smooth muscle increases the number and force of muscle contractions.

Terminals of postganglionic fibers of the sympathetic system release norepinephrine, which interacts with a- and ft-adrenergic receptors located on the effectors. Once again, it is impossible to assign a general response to agonist-receptor interaction. Stimulation of ft-adren-ergic receptors on the heart increases both heart rate and the force of contraction, whereas activation of ft-adrenergic receptors on intestinal smooth muscle decreases the number and force of contractions.

A specific listing of responses that can be induced in each organ of the body by the sympathetic and parasympathetic nervous systems or by drugs that act on autonomic receptors is not presented in this chapter; such information is presented in the chapters on individual organ systems. Also, additional information is available in pharmacology texts. Many pharmacologic agents have been developed to act preferentially on specific receptors located in the tissue or tissues of one or more organs. The ft-adrenergic receptor antagonist propranolol, for example, is often prescribed for the treatment of certain forms of cardiac arrhythmias because it competes with the binding of endogenously released catecholamines to ft-adrenergic receptors located in the heart. However, because propranolol will also block ft-adrenergic receptors located on airway smooth muscle, resulting in airway constriction, it is not desirable to prescribe propranolol in patients with airway disease. This lack of selectivity has led to the development of drugs such as metoprolol that preferentially block cardiac ft1-adrenergic receptors over the ft2-adrenergic receptors of the respiratory system.

Thus, the diversity and specificity of action of the ANS on the various organs of the body are due to several factors (see Fig. 3): (1) the discrete anatomic organization and projection of its sympathetic and parasympathetic divisions, (2) the presence of multiple neurotransmitters within each division, and (3) the presence of multiple receptors for those transmitters within effector organs.

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