Inhibition of Captopril-induced Increase in Plasma Renin Activity by Propranolol

抄録

The inhibition of renin release by angiotensin II (AII) is well documented. However, the interaction of this short loop feedback mechanism of AII with the sympathetic nervous system is still unclear. This study was designed to investigate the possible functional relationship between AII and the beta-adrenergic receptors with respect to renin release in vivo. First, the effect of propranolol on captopril-induced renin release was examined in conscious . rats. Secondly, the effect of AII on isoproterenol-induced renin release was determined. Captopril (1mg/Kg) increased plasma renin activity (PRA) from 1.6±0.3ng/ml/hr to 4.5±0.6ng/ml/hr (p<0.01). In contrast, there was no significant change in PRA in rats which received both captopril and propranolol (before 0.9±0.2ng/ml/hr, after 1.3±0.3ng/ml/hr). Thus, propranolol attenuated the increase in PRA caused by captopril.
Isoproterenol infusion (0.1μg/Kg/min) provoked a significant increase in PRA (before 1.3±0.4ng/ml/hr, after 6.6±1.7ng/ml/hr, p<0.01). AII infusion in combination with isoproterenol also increased PRA from 1.6±0.4ng/ml/hr to 5.2±0.3ng/ml/hr (p<0.01). AII in this dose did not suppress isoproterenol-induced renin release. These results suggest that the beta-adrenergic receptor mediating renin release is functionally located distal to the AII receptor in the short loop mechanism controlling renin release.