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(Hypertension. 2003;42:523.)
© 2003 American Heart Association, Inc.

Scientific Contributions

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

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.

Correspondence to Sandford L. Skinner, MD, Department of Physiology, University of Melbourne, Victoria 3010, Australia. E-mail s.skinner{at}physiology.unimelb.edu.au

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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