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신동맥내 투여한 Angiotensin II가 신장기능 및 Renin 분비에 미치는 영향
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  • 신동맥내 투여한 Angiotensin II가 신장기능 및 Renin 분비에 미치는 영향
  • Effect of Unilateral Renal Arterial Infusion of Angiotensin II on Renal Function and Renin Secretion in Unanesthetized Rabbit
저자명
김종훈(Kim, Jong-Hun),강남부(Kang, Nam-Poo),김영진(Kim, Young-Jin),김선희(Kim, Suhn-Hee),조경우(Cho, Kyung-Woo)
간행물명
대한생리학회지
권/호정보
1989년|23권 2호(통권44호)|pp.363-376 (14 pages)
발행정보
대한생리학회|한국
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정기간행물|KOR|
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영문초록

It has been well known that peripheral infusion of angiotensin II results in an increase of blood pressure, and an elevation of aldosterone secretion, and an inhibition of renin relase. However, the direct effect of angiotensin II on renal function has not been clearly established. In the present study, to investigate the effect of angiotensin II on renal function and renin release, angiotensin II (0.3, 3 and 10 ng/kg/min) was infused into a unilateral renal artery of the unanesthetized rabbit and changes in renal function and active and inactive renin secretion rate (ARSR, IRSR) were measured. In addition, to determine the relationship between the renal effect of angiotensin II and adenosine, the angiotensin II effect was evaluated in the presence of simultaneously infused 8-phenyltheophylline (8-PT, 30 nmole/min), adenosine A 1 receptor antagonist. Angiotensin II infusion at dose less than 10 ng/kg/min decreased urine flow, clearances of para-amino-hippuric acid and creatinine, and urinary excretion of electrolytes in dose-dependent manner. The changes in urine flow and sodium excretion were significantly correlated with the change in renal hemodynamics. Infusion of angiotensin II at 10 ng/kg/min also decreased ARSR, but it has no significant effect on IRSR. The change in ARSR was inversely correlated with the change in IRSR. The plasma concentration of catecholamine was not altered by an intarenal infusion of angiotensin II. In the presence of 8-PT in the infusate, the effect of angiotensin II on renal function was significantly attenuated, but that on renin secretion was not modified. These results suggest that the reduction in urine flow and Na excretion during intrarenal infusion of angiotensin II was not due to direct inhibitions of renal tubular transport systems, but to alterations of renal hemodynamics which may partly be mediated by the adenosine receptor.

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