Minoxidil controlled blood pressure (130 vs 187 mmHg, P<0.001) but did not reduce ventricular weight, indicating blood pressure control may not be the sole factor for reversing cardiac hypertrophy.
Absolute Event Rate: 130% vs 187%
p-value: p=<0.001
Biochemical (myocardial DNA, RNA, and hydroxyproline) and humoral (plasma PRA and kidney KRA renin activity) factors were determined in spontaneously hypertensive rats (SHR) and normotensive Wistar controls (NR) before and following treatment with minoxidil or propranolol. Minoxidil (150 mg.litre-1 drinking water) effectively controlled blood pressure (17.3 kPa vs 24.9 kPa 130 mmHg vs 187 mmHg, P less than 0.001) despite marked and sustained increases in both PRA and KRA ventricular weight which were not reduced and myocardial DNA, RNA, and hyperdroxyproline which were increased by minoxidil (P less than 0.01). In contrast propranolol did not reduce blood pressure in SHR but ventricular weight was reduced somewhat (3.1 +/- 0.4 mg.g-1 vs 3.4 +/- 0.09 mg.g-1, P less than 0.05); in both SHR and NR, KRA, and PRA were lowered by pranolol. Methyldopa which controlled blood pressure and lowered PRA led to a reversal of hypertrophy. Thus, although blood pressure control is obviously important for reversing cardiac hypertrophy, it may not be the sole factor for the development and reversal of cardiac hypertrophy.
Sen et al. (Thu,) conducted a other in Hypertension and cardiac hypertrophy. Minoxidil, propranolol, or methyldopa vs. Untreated controls was evaluated on Blood pressure (mmHg) (p=<0.001). Minoxidil controlled blood pressure (130 vs 187 mmHg, P<0.001) but did not reduce ventricular weight, indicating blood pressure control may not be the sole factor for reversing cardiac hypertrophy.