EFFECT OF BILATERAL-NEPHRECTOMY ON ACTIVE RENIN, ANGIOTENSINOGEN, ANDRENIN GLYCOFORMS IN PLASMA AND MYOCARDIUM

In an attempt to clarify the relationship of the circulating and myoca rdial renin-angiotensin systems, active renin concentration, its const ituent major glycoforms (active renin glycoforms I through V), and ang iotensinogen were measured in plasma and left ventricular homogenates from sodium-depleted rats under control conditions or 2 minutes, 3 hou rs, 6 hours, and 48 hours after bilateral nephrectomy (BNX). Control m yocardial renin concentration was 1.4+/-0.1 ng angiotensin I (Ang I) p er gram myocardium per hour and plasma renin concentration was 6.7+/-1 .1 ng Ang I per milliliter plasma per hour. Control myocardial angiote nsinogen was 0.042+/-0.004 mu mol/kg myocardium and plasma angiotensin ogen was 1.5 mu mol/L plasma. Two minutes after BNX and corresponding stimulation of renin secretion by anesthesia and surgery, plasma renin concentration was increased disproportionately compared with myocardi al renin. Three, 6, and 48 hours after BNX, renin decay occurred signi ficantly 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 in creased 12-fold and plasma angiotensinogen concentrations had increase d by only 3.5-fold. Myocardial renin glycoform proportions were identi cal in myocardial homogenates and plasma in control animals. At 6 hour s BNX, the proportions of plasma active renin glycoforms I+II fell, wh ile those in the myocardium significantly increased. We conclude that in control rats, active renin and active renin glycoforms are distribu ted as if in diffusion equilibrium between plasma and the myocardial i nterstitial space. After BNX, myocardial renin concentration falls dra matically, suggesting that most cardiac renin is derived from plasma r enin of renal origin. After BNX, renin glycoforms I+II are preferentia lly cleared from the plasma but preferentially retained by the myocard ium. Control myocardial angiotensinogen concentrations are too low to result from simple diffusion equilibrium between plasma and the myocar dial interstitium.