The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (P-DA) and systemic vascular resistance (R-S), and significant increases in plasma angiotensin II (Ang II) and catecholanline concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented P-DA and R-S recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented P-DA and R-S recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in P-DA and R-S, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril + papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in P-DA and R-S. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have: important roles in the: compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to P-DA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines.
