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a1 aj-oxymetazoline

^-isoproterenol a, ci2 P1 ^-epinephrine a, Oz Pi -norepinephrine ephedrine (a-f otg P2 and releasing agent)

amphetamine cocaine tyramine pargyline entacapone

Responses are not reduced by prior treatment with reserpine or guanethidine. Response may be potentiated by cocaine, reserpine, and guanethidine.

Response is reduced by prior treatment with reserpine or guanethidine.

Responses are abolished by prior treatment with reserpine or guanethidine.

FIGURE 10-1 Classification of adrenergic receptor agonists and drugs that produce sympathomimetic effects. For each category, a prototypical drug is shown. *Not actually sympathetic drugs but produce sympathomimetic effects.

are potent bronchodilators. Cutaneous blood vessels physiologically express almost exclusively a receptors; thus, NE and Epi cause constriction of such vessels, whereas isoproterenol has little effect. The smooth muscle of blood vessels that supply skeletal muscles has both b2 and a receptors; activation of b2 receptors causes vasodilation, and stimulation of a receptors constricts these vessels. In such vessels, the threshold concentration for activation of b2 receptors by Epi is lower than that for a receptors, but when both types of receptors are activated at high concentrations of Epi, the response to a receptors predominates; physiological concentrations of Epi primarily cause vasodilation.

The integrated response of an organ to sympathomimetic amines results not only from their direct effects, but also from reflex homeostatic adjustments. A striking effect of many sympathomimetic amines is a rise in arterial blood pressure caused by stimulation of vascular a adrenergic receptors. This stimulation elicits compensatory reflexes (mediated by the carotid—aortic baroreceptor system) that adjust CNS outflow to the cardiovascular system. As a result, sympathetic tone is diminished and vagal tone is enhanced; each of these responses leads to slowing of the heart rate. Conversely, when a drug (e.g., a b2 agonist) lowers mean blood pressure at the mechanoreceptors of the carotid sinus and aortic arch, the baroreceptor reflex works to restore pressure by reducing parasympathetic (vagal) outflow from the CNS to the heart, and increasing sympathetic outflow to the heart and vessels. The baroreceptor reflex effect is of special importance for drugs that have little capacity to activate b receptors directly. With diseases (e.g., atherosclerosis) that may impair baroreceptor mechanisms, effects of sympathomimetic drugs may be magnified.

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