Transmission of impulses across the nerve terminal junctional sites (synaptic cleft) of the peripheral ANS occurs through the mediation of liberated chemicals (neurotransmitters). These neurotransmitters interact with a receptor on the end organ to evoke a biologic response.
Acetylcholine (ACh) is the neurotransmitter at preganglionic nerve endings of the SNS and PNS and at postganglionic nerve endings of the PNS.
The ability of a receptor to modulate the function of an effector organ depends on rapid recovery to its baseline state after stimulation. ACh removal occurs by rapid hydrolysis by acetylcholinesterase (true cholinesterase). Pseudocholinesterase (plasma cholinesterase) is not physiologically significant in the termination (hydrolysis) of ACh action.
Sympathetic Nervous System Neurotransmission
Norepinephrine is the neurotransmitter at postganglionic nerve endings of the SNS (except in the sweat glands, where ACh is the neurotransmitter).
Adenosine triphosphate (ATP) is released with norepinephrine and thus functions as a co-neurotransmitter.
Epinephrine is the principal hormone released by chromaffin cells (which function as postganglionic SNS neurons) into the circulation to function as a neurotransmitter hormone.
Endogenous catecholamines are dopamine (neurotransmitter in the CNS), norepinephrine, and epinephrine. A catecholamine (including synthetic catecholamines) is any compound with a catechol nucleus (benzene ring with two adjacent hydroxyl groups) and an amine-containing side chain (Fig. 15-3: Synthesis of catecholamines).
The effects of endogenous or synthetic catecholamines on adrenergic receptors can be indirect (little intrinsic activity but stimulate release of stored neurotransmitter) and direct.
Inactivation of catecholamines is by reuptake back into presynaptic nerve terminals by extraneuronal uptake, diffusion, and metabolism.