Cardiac Hypertrophy in Spontaneously Hypertensive Rats

TLDR

The study administered methyldopa and hydralazine to younger rats to prevent hypertension, yielding comparable outcomes. Spontaneously hypertensive rats show increased ventricular weight and reduced DNA concentration, with plasma renin activity rising before hypertension and correlating with hypertrophy; methyldopa lowers both ventricular weight and renin activity, whereas hydralazine does not, suggesting blood pressure alone does not drive hypertrophy and the renin‑angiotensin system may enhance myocardial growth.

Abstract

Ventricular weight in spontaneously hypertensive rats (F26 generation, Okamoto-Aoki strain) was significantly higher ( P < 0.001) than that in body weight-matched American Wistar and Kyoto-Wistar normotensive rats, not only among older groups of rats but also among younger groups that had not developed significant hypertension. Deoxyribonucleic acid (DNA) concentration in ventricular muscle was not different from normal in the youngest group ( P < 0.4) but was significantly reduced in the older spontaneously hypertensive rats ( P < 0.01). Plasma renin activity was significantly increased in younger spontaneously hypertensive rats before the development of established hypertension; moreover, ventricular weight and plasma renin activity were significantly correlated in younger rats ( r = 0.788, P < 0.005 for all rats, r = 0.644, P < 0.01 for spontaneously hypertensive rats). Antihypertensive therapy with either α-methyldopa or hydralazine reduced blood pressure, especially in hypertensive rats; however, ventricular weight was reduced by methyldopa ( P < 0.01) but not by hydralazine. Plasma renin activity was reduced by methyldopa but increased by hydralazine ( P < 0.01). DNA concentration was reversed toward normal by methyldopa but not by hydralazine. Similar results were obtained when methyldopa and hydralazine were given to younger rats to prevent hypertension. The changes in ventricular weight with the onset of hypertension and with its reversal or its prevention suggest that blood pressure might not be the sole factor contributing to cardiac hypertrophy in the spontaneously hypertensive rat and that the renin-angiotensin system might play a permissive role enhancing myocardial hypertrophy.