Evidence for the existence of vascular alpha 2-adrenergic receptors in humans.

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Abstract
Many studies have suggested that .alpha.-adrenergic receptors on vascular smooth muscle are heterogeneous and that both .alpha.1- and .alpha.2-adrenergic receptors can cause vasoconstriction when stimulated. This hypothesis was explored in normal humans by comparing the capacity of yohimbine, and .alpha.2-adrenergic receptor antagonist, parazosin and .alpha.1-adrenergic receptor antagonist, with differentially blocked pressor responses to phenylephrine, and .alpha.1-adrenergic receptor agonist and epinephrine, a nonselective .alpha.-agonist. These responses were studied in normal male volunteers who were pretreated with propranolol (80 mg orally every 8 h for 5 days) to obviate stimulation of .beta.-receptors by either agonist. Differential effects of the antagonists on responses to the 2 agonists were found. Yohimbine induced a 3.1-fold (.+-. 0.5) shift in the dose of epinephrine, which raised blood pressure 25 mm Hg, and only a 1.9-fold (.+-. 0.2) shift in the response to phenylephrine (P < 0.01). Prazosin induced a 2.4-fold (.+-. 0.5) shift in the responses to epinephrine and a 4.5-fold (.+-. 1.2) shift in the response to phenylephrine (P < 0.05). These data are consistent with the motion that .alpha.-adrenergic receptors in the human vasculature are not homogeneous, but rather may be subdivided into at least 2 subtypes, 1 resembling .alpha.1-adrenergic receptors and the other resembling .alpha.2-adrenergic receptors.