Key result
The kinetic constants for purified mouse Ren-2 renin reacting with rat angiotensinogen were not different from rat renin, indicating that hypertension in the Ren-2 rat is not related to renin kinetics.
Hypertension in the Ren-2 rat is not explained by enhanced kinetics of transgenic Ren-2 renin reacting with endogenous rat angiotensinogen.
Does not implicate renin kinetics in Ren-2 rat hypertension; leaves open alternative mechanisms for investigation.
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 micromol/L). Under these conditions, the kinetic constants for Ren-2 (Km, 1.8 micromol/L; Kcat, 0.07/s; and Kcat/Km, 0.04 L x micromol(-1) x 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.
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Rong et al. (2003) studied Hypertension in the (mRen-2)27 transgenic rat. Purified mouse Ren-2 renin vs. Rat renin was evaluated on Kinetic constants (Km, Kcat, Kcat/Km) reacting with physiologic concentrations of rat angiotensinogen. The kinetic constants for purified mouse Ren-2 renin reacting with rat angiotensinogen were not different from rat renin, indicating that hypertension in the Ren-2 rat is not related to renin kinetics.
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