I

Smooth Muscle Cells

Contraction

FIGURE 5 Various excitatory (+) and inhibitory (-) receptor mechanisms located on sympathetic varicosities. ACh, acetylcholine; a, a-adrenergic receptor; AT, angiotensin II; H2, histamine2 receptor; 5-HT, 5-hydroxytryptamine; M, muscarinic receptor; NE, norepi-nephrine; PC, prostacyclin; PGE1, prostaglandin E1; ?, unknown mechanism. (Modified from McGrath MA, Vanhouette PM, in Vanhouette PM, Leusen S, Eds., Mechanisms of vasodilation. Basel: S. Karger, 1978, pp. 248-257.)

FIGURE 6 Mechanisms affecting the concentration of norepinephrine (NE) within the junctional cleft available for binding to a receptor (R) on an effector cell. Norepinephrine is removed by (A) neuronal uptake, in which some is degraded by monoamine oxidase (MAO) to 3,4-dihydroxyphenylglycol (DOPEG), but most is restored in vesicles; (B) diffusion into capillaries; and (C) uptake into effector cells and subsequent degradation by the enzymes MAO and catechol-O-methyltransferase (COMT) to 3,4-dihydroxymandelix acid (DOMA), normetanephrine (NMN), 3-methoxy-4-dihydroxyphenylglycol (MOPEG), and 3-methoxy-4-hydroxymandelic acid (VMA). These metabolites are inactive and diffuse into the extracellular fluid and the capillaries. Neuronal uptake of norepinephrine is mediated by an active transport.

FIGURE 6 Mechanisms affecting the concentration of norepinephrine (NE) within the junctional cleft available for binding to a receptor (R) on an effector cell. Norepinephrine is removed by (A) neuronal uptake, in which some is degraded by monoamine oxidase (MAO) to 3,4-dihydroxyphenylglycol (DOPEG), but most is restored in vesicles; (B) diffusion into capillaries; and (C) uptake into effector cells and subsequent degradation by the enzymes MAO and catechol-O-methyltransferase (COMT) to 3,4-dihydroxymandelix acid (DOMA), normetanephrine (NMN), 3-methoxy-4-dihydroxyphenylglycol (MOPEG), and 3-methoxy-4-hydroxymandelic acid (VMA). These metabolites are inactive and diffuse into the extracellular fluid and the capillaries. Neuronal uptake of norepinephrine is mediated by an active transport.

Diffusion of transmitter away from the target cells is enhanced by the fact that the junctional cleft between the varicosities and the effector cells is large compared with the junctional cleft between somatic neurons and end plates of skeletal muscles.

The mechanisms available for modulating the concentration of ACh in the junctional clefts between terminals of parasympathetic postganglionic neurons and effector cells are not as varied as those associated with sympathetic adrenergic neurotransmission. Some parasympathetic postganglionic axons have terminal regions lined with varicosities, and others have single boutons at their ends. A bouton-type ending and its mechanisms for regulating ACh in the junctional cleft are illustrated in Fig. 7. Action potentials arriving at the bouton induce an influx of Ca2+ ions, triggering the release of ACh from the synaptic vesicles into the cleft. ACh in the cleft is degraded by acetylcholinesterase into choline and acetate. Some of the choline is taken up by the bouton and resynthesized into ACh.

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