Potentiation of Renin Release by Combining Renal Arterial Constriction and β -Adrenergic Stimulation

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Abstract
Intrarenal mechanisms for renin release can be activated by reducing renal arterial pressure until renal blood flow (RBF) falls, but renin release is not further raised by reducing arterial pressure below the range of autoregulation of RBF. To examine whether the renin release evoked by reduction of renal arterial pressure is influenced by adrenergic stimulation, isoproterenol or propranolol was administered in anesthetized dogs at control pressure (120-140 mm Hg) and after constricting the renal artery to a low pressure (50-60 mm Hg), well below the range of autoregulation of RBF. Infusion of isoproterenol into the renal artery (0.2 μg/min per kg body weight) increased renin release from 1.8 ± 0.5 μg/min (mean ± S.E.M.) to 8.9 ± 1.7 μg/min at control pressure and from 31.9 ± 3.2 μg/min to 54.3 ± 5.0 μg/min at low pressure. Thus, isoproterenol raised renin release more (P < 0.05) at low (δRR = 22.4 ± 2.9 μg/min) than at normal renal arterial pressure (δRR = 7.1 ± 1.6 μg/min). Similar results were obtained by intravenous infusion. Blockade of β-receptors with propranolol reduced renin release from 2.1 ± 0.8 μg/min to 0.5 ± 0.4 μg/min at control pressure and from 43.8 ± 10.9 μg/min to 27.9 ± 4.2 μg/min at low renal arterial pressure. Propranolol inhibited renin release more (P < 0.05) at low (δRR = −15.9 ± 8.3 μg/min) than at control renal arterial pressure (δRR = −1.6 ± 0.8 μg/min). It is concluded that the combination of low renal arterial pressure and high sympathetic β-receptor activity potentiates renin release.

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