書誌事項
- タイトル別名
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- Is renal renin release mediated through .BETA.1- or .BETA.2-adrenoceptors?
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説明
The present study was undertaken to investigate whether renal renin release is mediated through β1- or β2-adrenoceptors. Various β agonists were infused into Wistar male rats with catheters indwelled in the femoral artery and vein under consciousness without restriction. Plasma renin activity (PRA) increased 2.5 or 3.6 times in response to isoproterenol infusion for 10 min at 125 ng/kg/min or β1-selective prenalterol infusion at 1, 875 ng/ kg/min, respectively. Both β agonists resulted in a singnificant increase in heart rate, but not blood pressure. Beta2-adrenergic agent, terbutaline, also demonstrated 4.2-fold increase in PRA at 62.5 ng/kg/min, while blood pressure and heart rates were not changed significantly. On the other hand, atenolol, β1-antagonist (3 mg/kg, i, v.) markedly suppressed PRA up to 21 to 23% of the initial levels without any changes in blood pressure and heart rate, for a period of 30 to 40 min after a bolus injection of 3.0 mg/kg. The pretreatment of rats with the same dosage of atenolol completely abolished terbutaline-induced RRA rise. In addition, preceding administration of a selective β2-blocker, ICI 118, 551 (3 mg/ kg, i, v.), totally inhibited an increase in PRA stimulated by terbutaline. The results suggest that renal renin release is stimulated mainly through β1-adreno-ceptors and terbutaline-induced renin release may be mediated through vasodilatory β2 action on vascular beds, which in turn activates sympathetic nervous tone.
収録刊行物
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- 日本腎臓学会誌
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日本腎臓学会誌 30 (10), 1165-1170, 1988
社団法人 日本腎臓学会
