(Hypertension. 1997;30:259-266.)
© 1997 American Heart Association, Inc.
Articles |
Effect of Bilateral Nephrectomy on Active Renin, Angiotensinogen, and Renin Glycoforms in Plasma and Myocardium
From the Division of Nephrology, Hennepin County Medical Center (S.A.K., J.A.O., L.M.F.), Minneapolis, Minn; and the Departments of Physiology (S.A.K.) and Medicine (J.A.O., A.T.H.) and the Vascular Medicine Program, Minnesota Vascular Diseases Center (M.M.L., A.T.H.), University of Minnesota Medical School, Minneapolis.
Correspondence to Stephen A. Katz, Associate Professor of Physiology, University of Minnesota School of Medicine and Senior Investigator, Hennepin County Medical Center, Division of Nephrology, D Bldg, 5th Floor, 701 Park Ave, Minneapolis, Minnesota 55415-1829. E-mail katzx001{at}maroon.tc.umn.edu
Abstract In an attempt to clarify the relationship of the circulating and myocardial renin-angiotensin systems, active renin concentration, its constituent major glycoforms (active renin glycoforms I through V), and angiotensinogen were measured in plasma and left ventricular homogenates from sodium-depleted rats under control conditions or 2 minutes, 3 hours, 6 hours, and 48 hours after bilateral nephrectomy (BNX). Control myocardial renin concentration was 1.4±0.1 ng angiotensin I (Ang I) per gram myocardium per hour and plasma renin concentration was 6.7±1.1 ng Ang I per milliliter plasma per hour. Control myocardial angiotensinogen was 0.042±0.004 µmol/kg myocardium and plasma angiotensinogen was 1.5 µmol/L plasma. Two minutes after BNX and corresponding stimulation of renin secretion by anesthesia and surgery, plasma renin concentration was increased disproportionately compared with myocardial renin. Three, 6, and 48 hours after BNX, renin decay occurred significantly faster from the plasma than from the myocardium. Forty-eight hours after BNX, myocardial renin concentrations had fallen to 15% of control values, while myocardial angiotensinogen concentrations had increased 12-fold and plasma angiotensinogen concentrations had increased by only 3.5-fold. Myocardial renin glycoform proportions were identical in myocardial homogenates and plasma in control animals. At 6 hours BNX, the proportions of plasma active renin glycoforms I+II fell, while those in the myocardium significantly increased. We conclude that in control rats, active renin and active renin glycoforms are distributed as if in diffusion equilibrium between plasma and the myocardial interstitial space. After BNX, myocardial renin concentration falls dramatically, suggesting that most cardiac renin is derived from plasma renin of renal origin. After BNX, renin glycoforms I+II are preferentially cleared from the plasma but preferentially retained by the myocardium. Control myocardial angiotensinogen concentrations are too low to result from simple diffusion equilibrium between plasma and the myocardial interstitium.
Key Words: renin • myocardium • renin glycoforms • angiotensinogen • renin-angiotensin system
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