Angiotensinogen's role in ANG formation, renin release, and renal hemodynamics in isolated perfused kidney.

Isolated perfused rat kidneys were used to investigate the effects of the addition of pure angiotensinogen or renin-free plasma to the perfusate on angiotensin I (ANG I) and angiotensin II (ANG II) generation, renal hemodynamics, and renin release. When no angiotensinogen or plasma is added, a very small amount of angiotensinogen is initially detected in the perfusate. Whereas renin secreted by the kidney accumulates in the perfusate, angiotensinogen disappears during the perfusion and immunoreactive ANG II cannot be detected. The addition of angiotensinogen reactivates the renin-angiotensin system. ANG I, [des-Asp1] ANG I, ANG II, and [des-Asp1] ANG II are progressively generated in the perfusate. At a constant perfusion pressure, as well as at a variable perfusion pressure, a progressive fall in renal perfusate flow is observed that is significantly correlated to the level of immunoreactive ANG II. ANG II significantly blunts the rise in renin, and renin release in the perfusate is negatively correlated to immunoreactive ANG II levels. Comparison of the ANG I and ANG II levels in in vitro incubated perfusates and circulated perfusates shows that in plasma-injected perfusates the level of immunoreactive ANG II is dependent on both the production of ANG I and its conversion to ANG II by renal and perfusate converting-enzyme activity, and on ANG I and ANG II degradation by the kidney and the perfusate.