Progression and regression of cardiac hypertrophy in hypertensive rats: biochemical and molecular changes in ventricular myosin.
We investigated the changes in ventricular isomyosin composition and Ca2+-activated ATPase activity during progression and regression of hypertension and cardiac hypertrophy. Eight control male Wistar rats and 14 Goldblatt-II (two-kidney, one clip) hypertensive rats were studied from the 5th week of age. Five of the Goldblatt-II rats underwent nephrectomy of the ischaemic kidney after 5 weeks, with normalization of blood pressure. The hypertensive rats showed a higher biventricular weight to body weight ratio (P less than 0.02), a lower ATPase activity (P less than 0.005), and an increased expression of 'slow' isomyosins in comparison with the age-matched controls. These changes were more pronounced at 15 than at 10 weeks of age. The 15-week-old nephrectomized rats showed the same degree of cardiac hypertrophy, ATPase activity and isomyosin pattern as the age-matched controls. In conclusion, the changes in ventricular myosin observed during the progression of cardiac hypertrophy regressed after normalization of blood pressure and ventricular mass.
D000818:Animals; D001794:Blood Pressure; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology* / Q000378:metabolism; D006978:Hypertension, Renovascular / Q000150:complications / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D009218:Myosins; D000252:Calcium-Transporting ATPases