Published Online
on September 29, 2003

A more recent version of this article appeared on October 1, 2003

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Submitted on March 11, 2003
Revised on April 3, 2003

Hypertension in the (mRen-2)27 Rat Is Not Explained by Enhanced Kinetics of Transgenic Ren-2 Renin

Pei Rong; Duncan J. Campbell; and Sandford L. Skinner^*

From the Department of Physiology (P.R., S.L.S.) and St Vincent's Institute of Medical Research and Department of Medicine (D.J.C), University of Melbourne, Melbourne, Australia.

^* To whom correspondence should be addressed. E-mail: s.skinner{at}physiology.unimelb.edu.au.

Abstract--Enhanced efficiency of the reaction between transgenic Ren-2 mouse renin and endogenous rat angiotensinogen has been suggested as 1 mechanism that contributes to the accelerated hypertension and increased tissue angiotensin of the (mRen-2)27 transgenic rat. This was tested in a study conducted at pH 7.4 in vitro that compared the kinetic constants of purified mouse Ren-2 and rat renin (each at 100, 75, 50, and 25 pmol/L) reacting with physiologic concentrations of rat angiotensinogen (0 to 4 µmol/L). Under these conditions, the kinetic constants for Ren-2 (K_m, 1.8 µmol/L; K_cat, 0.07/s; and K_cat/K_m, 0.04 L · µmol^-1 · s^-1) were not different from rat renin. However, Ren-2 renin acting on its homologous mouse angiotensinogen was confirmed as being much slower. We conclude that hypertension in the Ren-2 rat is not related to renin kinetics. Other mechanisms are considered, with reference to human essential hypertension.

Key words: renin-angiotensin system • angiotensinogen • blood pressure • hypertension, essential

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