The cardiovascular effects of norepinephrine, epineph-rine, and isoproterenol are shown in Table 10.1. Differences in the action of these three catecholamines on various vascular beds are due both to the different affinities possessed by the catecholamines for a- and p-adrenoceptors and to differences in the relative distribution of the receptors in a particular vascular bed. The hemodynamic responses of the major vascular beds to these amines are shown in Table 10.2.
The blood vessels of the skin and mucous membranes predominantly contain a-adrenoceptors. Both epinephrine and norepinephrine produce a powerful constriction in these tissues, substantially reducing blood flow through them. Isoproterenol, which is almost a pure p-adrenoceptor agonist, has little effect on the vasculature of the skin and mucous membranes. The blood vessels in visceral organs, including the kidneys, contain predominantly a-adrenoceptors, although some p2-adrenoceptors are also present. Consequently, epi-nephrine and norepinephrine cause vasoconstriction and reduced blood flow through the kidneys and other visceral organs. Isoproterenol produces either no effect or weak vasodilation.
The blood vessels in skeletal muscle contain both a-and p2-adrenoceptors. Norepinephrine constricts these blood vessels and reduces blood flow through an interaction with a-adrenoceptors. Isoproterenol dilates the vessels in skeletal muscle and consequently increases blood flow through the tissue by interaction with the p2-adrenoceptors. Epinephrine has a more complex ac-
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