Cardiac hypertrophy and antihypertensive therapy.
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.
D000818:Animals; D006332:Cardiomegaly / Q000188:drug therapy*; D004247:DNA / Q000378:metabolism; D006909:Hydroxyproline / Q000378:metabolism; D006973:Hypertension / Q000188:drug therapy*; D008297:Male; D008750:Methyldopa / Q000627:therapeutic use; D008914:Minoxidil / Q000627:therapeutic use*; D009206:Myocardium / Q000378:metabolism; D011433:Propranolol / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D012313:RNA / Q000378:metabolism; D051381:Rats; D012083:Renin / Q000378:metabolism
D011743:Pyrimidines; D008750:Methyldopa; D008914:Minoxidil; D012313:RNA; D004247:DNA; D011433:Propranolol; D012083:Renin; D006909:Hydroxyproline