ADRENAL BLOOD-FLOW AND SECRETORY EFFECTS OF ADRENERGIC-RECEPTOR STIMULATION

To evaluate effects of adrenergic receptor stimulation on regional adr enal blood flow and secretion, pentobarbital-anesthetized dogs (n = 5- 6/group) received the beta-agonist isoproterenol (group I), the al-ago nist 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 we re made before and during agonist infusion. Isoproterenol increased ca techolamine secretion but had no direct effect on MQ or CQ. In contras t, phenylephrine increased MQ and CQ. four- and twofold, respectively. Dexmedetomidine had no effect on MQ or catecholamine secretion. To ev aluate whether blood flow effects of phenylephrine were due to increas es in mean arterial blood pressure (MAP) or related to activation of a l-adrenergic receptors, two additional groups of animals received phen ylephrine; group IV had MAP maintained at baseline by controlled hemor rhage into a pressurized bottle; group V received prazosin before phen ylephrine. 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 l igand, I-125-labeled [beta-(4-hydroxyphenyl)ethlamino-methyl]tetralone , demonstrated specific and saturable bind 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 stimu lation. The mechanism responsible for this vasodilation is not known.