A differential effect of yohimbine on adrenal and neuronal catecholamine release during bilateral carotid occlusion in the dog.

ABSTRACT

This study reports on the effects of yohimbine and clonidine on the release of adrenal and renal catecholamines (epinephrine, E; norepinephrine, NE; and dopamine, DA) in response to bilateral carotid occlusion (BCO, 3 min) in vagotomized dogs anesthetized with sodium pentobarbital. The model used allowed us to simultaneously compare adrenal catecholamine secretion with neuronal NE release in the kidney. In control dogs, the net output (ng/min/g tissue) of adrenal E (70.5 +/- 19.7), NE (22.2 +/- 5.9) and DA (2.6 +/- 0.8) increased markedly (P less than 0.01) during BCO to a maximum level of 265.1 +/- 87.9, 97.4 +/- 30.6 and 10.5 +/- 3.2, respectively. Similarly, the net output (ng/min/g tissue) of renal NE (0.66 +/- 0.06) and DA (0.09 +/- 0.02) increased significantly (P less than 0.01) to 1.00 +/- 0.11 and 0.15 +/- 0.04, respectively. Aortic systolic pressure (mm Hg) (140.8 +/- 8.0) and heart rate (beats/min) (162.7 +/- 5.1) also increased (P less than 0.01) to 212.5 +/- 19.3 and 179.5 +/- 5.4, respectively. In dogs treated with yohimbine (0.3 mg/kg, i.v.), the net increase in adrenal catecholamine output was diminished by approximately 47% (P less than 0.05). In contrast, the net increase in renal NE output was potentiated by 41% (P less than 0.05). The net increase in heart rate was also enhanced significantly (P less than 0.01) in the presence of yohimbine. In dogs receiving clonidine (15 micrograms/kg, i.v.) the increases in net output of both adrenal and renal catecholamine were abolished. Similarly, pressor and heart rate responses were abolished in the presence of clonidine. The results indicate that yohimbine exerted a differential effect on renal sympathetic nerves (increase) and adrenal medullae (decrease) in modulating catecholamine release in response to BCO, while clonidine abolished both neural NE release and adrenal catecholamine secretion. This study suggests that a presynaptic alpha 2-adrenoceptor-mediated mechanism, the blockade of which enhances neural NE release at peripheral sympathetic nerve terminals in many tissues, may not be involved in the modulation of adrenal catecholamine secretion during BCO.