To evaluate effects of adrenergic receptor stimulation on regional adrenal blood flow and secretion, pentobarbital-anesthetized dogs (n = 5-6/group) received the beta-agonist isoproterenol (group I), the alpha 1-agonist phenylephrine (group II), or the alpha 2-agonist dexmedetomidine (group III). Measurements of adrenal cortical (CQ) and medullary (MQ) blood flow (radiolabeled microspheres) and catecholamine secretion were made before and during agonist infusion. Isoproterenol increased catecholamine secretion but had no direct effect on MQ or CQ. In contrast, phenylephrine increased MQ and CQ four- and twofold, respectively. Dexmedetomidine had no effect on MQ or catecholamine secretion. To evaluate whether blood flow effects of phenylephrine were due to increases in mean arterial blood pressure (MAP) or related to activation of alpha 1-adrenergic receptors, two additional groups of animals received phenylephrine; group IV had MAP maintained at baseline by controlled hemorrhage into a pressurized bottle; group V received prazosin before phenylephrine. Prevention of MAP increase did not prevent the vasodilation response to phenylephrine, but it was completely blocked by prazosin. Canine adrenal homogenates incubated with the alpha 1-adrenoceptor ligand, 125I-labeled 2-[beta-(4-hydroxyphenyl)ethlaminomethyl]tetralone, demonstrated specific and saturable binding, supporting the presence of alpha 1-adrenergic receptors. We conclude that increases in MQ and CQ elicited by phenylephrine appear to be due to alpha 1-receptor stimulation. The mechanism responsible for this vasodilation is not known.