Effect of antihypertensive treatment and N?? -nitro-L-arginine methyl ester on cardiovascular structure in deoxycorticosterone acetate-salt hypertensive rats

Abstract

These results suggest that the renin-angiotensin system does not play a role in cardiovascular hypertrophy in DOCA-salt hypertensive rats, which is not unexpected since plasma renin is suppressed in these rats. Calcium channel blockade may interfere with mechanisms underlying vascular hypertrophy in this model via blockade of calcium entry or by reducing vascular endothelin-1 gene expression when the blood pressure is lowered. L-NAME has been shown to exert a growth-inhibitory effect on small arteries and on the heart despite increasing blood pressure, probably independently from its ability to inhibit nitric oxide synthase, the latter of which is presumably involved in the blood pressure rise induced.