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MARK NICKERSON; Adrenergic Mediators. Invest. Ophthalmol. Vis. Sci. 1965;4(6):1085-1094.
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The only adrenergic mediator of importance in the control of the mammalian vascular system is noradrenaline, and its predominant effect is vasoconstriction, mediated by adrenergic α receptors. This vasoconstriction varies in degree depending on the vascular bed, the type of vessel, the degree of sympathetic innervation, and the physiologic state. Adrenaline released into the blood stream plays a negligible role in vascular responses. Present-day investigations of adrenergic control of the circulation, particularly studies in man, depend heavily on the use of drugs as pharmacologic tools. Agents are now available which are purported to act by causing the release of noradrenaline from endogenous stores, blocking tissue receptors, preventing release from or depleting sympathetic nerve endings of the mediator, inhibiting the synthesis of the mediator or causing displacement by a "false mediator," and preventing the loss of the mediator by uptake and storage in nerve endings. It is emphasized that none of these pharmacologic tools is entirely specific and that each response studied requires specific confirmation of a relationship between an assumed mechanism of drug action and an observed effect before valid conclusions can be drawn. Remits with agents preventing release from or depleting nerve endings of the mediator are particularly difficult to interpret. Although they remain obvious theoretical possibilities, none of the currently available agents has been shown to produce its effects by inhibiting noradrenaline synthesis or by causing the production of a false mediator. Inhibition of monoamine oxidase (MAO) does not alter most adrenergic responses and inhibition of catechol O-methyl transferase (COMT) has only limited effects, indicating that enzymatic inactivation plays no more than a minor role in terminating the effects of noradrenaline
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