Renal hemodynamics in the rat before and during inhibition of angiotensin II

• Published in: American journal of physiology. Renal physiology Vol. 233; no. 4; pp. F290 - F297
• Main Authors: Arendshorst, W J, Finn, W F
• Format: Journal Article
• Language: English
• Published: United States 01.10.1977
• Subjects: Angiotensin II - physiology; Animals; Blood Pressure; Diet; Glomerular Filtration Rate; Homeostasis; Kidney - blood supply; Kidney - physiology; Rats; Regional Blood Flow; Renin - physiology; Saralasin - pharmacology; Sodium - physiology; Teprotide - pharmacology; Vasomotor System - drug effects
• ISSN: 0002-9513; 1931-857X; 1522-1466
• DOI: 10.1152/ajprenal.1977.233.4.f290

Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow transducer in anesthetized rats which had been maintained for 3-5 wk on low, normal, or high salt plus deoxycorticosterone diets. After base-line observations, one of two dissimilar inhibitors of the renin-angiotensin system, angiotensin I converting enzyme inhibitor SQ 20881 or the structural analogue [Sar1,Ala8]angiotensin II was administered intravenously. The employed doses of SQ 20881 and [Sar1,Ala8]angiotensin II effectively inhibited the pressor and renal vasoconstrictor responses induced by exogenous angiotensin I and II, respectively, in each dietary group. Both inhibitors vasodilated kidneys in salt-restricted rats; however, neither affected base-line renal hemodynamics in salt-loaded rats. Pressure-flow relationships were evaluated by clamping the aorta to reduce renal perfusion pressure. Renal blood flow was autoregulated between 100 and 140 mmHg with the same efficiency before and during inhibition of angiotensin II in each dietary group. These data indicate that angiotensin II modifies base-line RBF and renal vascular resistance and are consistent with the view that the renin-angiotensin system is not an essential mechanism responsible for autoregulation of RBF in the rat.