Dual adrenergic control of renin during nonhypotensive hemorrhage in conscious dogs

These experiments evaluated the contribution of renal α-adrenoceptors, renal β-adrenoceptors, and extrarenal β-adrenoceptors to increased plasma renin activity (PRA) during nonhypotensive hemorrhage in conscious dogs. Blood withdrawal at a rate of 16 g/kg body wt over 20 min increased PRA to nearly threefold control levels without decreasing mean arterial pressure. The PRA response to hemorrhage was reduced to a greater extent by simultaneous direct renal arterial (ira) infusion of phenoxybenzamine and propranolol than by propranolol alone. Phenoxybenzamine infusion ira did not block α-adrenoceptors located outside of the kidney. The PRA and heart rate responses to hemorrhage were both significantly reduced when propranolol was infused either ira or intravenously (iv) at a rate of 2 μg·kg^-1·min^-1 for 20 min followed by 0.5 μg·kg^-1·min^-1 continuous infusion. Propranolol infusion at a lower rate (0.5 μg·kg^-1·min^-1 for 20 min followed by 0.12 μg·kg^-1·min^-1) had little effect on the magnitude of increase in PRA when infused either iv or ira. The calculated renal arterial plasma propranolol concentration was at least fivefold higher or more during ira than during iv propranolol infusion at each rate and was approximately the same during ira infusion at the lower rate (17.5 ± 0.7 ng/ml) as during iv infusion at the higher rate (16.7 ± 2.4 ng/ml). These data indicate that the hemorrhage-induced increase in PRA is mediated by renal α-adrenoceptors and extrarenal β-adrenoceptors, whereas renal β-adrenoceptors appear to play little or no role.