Correlation of myosin isoenzyme alterations with myocardial function in physiologic and pathologic hypertrophy.
To explore the interactions of physiologic and pathologic hypertrophy, four groups of hearts were studied in an isolated working rat heart apparatus. Cardiac contractile proteins were also evaluated. The groups were hearts of female control sedentary rats; rats subjected to a 10-week swimming programme; rats with renal hypertension; and hypertensive rats subjected to a 10-week swimming programme. The swimming programme in normotensive female rats caused a 30% cardiac hypertrophy, in hypertensive animals 46% hypertrophy, and in combined hypertension and swimming 70% hypertrophy. Ca2+-myosin ATPase activity and actin-activated myosin ATPase were elevated in hearts of swimmers, depressed in hearts of hypertensive sedentary animals and similar to control values in hearts of hypertensive swimmers. Myosin V1 isoenzyme content was increased in hearts of swimmers, depressed in hearts of hypertensives, but normal in hearts of hypertensive swimmers. Reciprocal relationships were seen with the V3 isoenzyme. Stroke work, mean velocity of circumferential fibre shortening, and per cent fractional shortening at the midwall showed increased values for hearts of swimmers, depressed values for hearts of hypertensives, and normal values or values above the control for hearts of hypertensive swimmers. Myocardial flow measured with microspheres was increased in the left ventricle of swimmers, depressed in hearts of hypertensives and still depressed in hypertensive swimmers, but significantly higher than in the hypertensives alone. The correlation of actin-activated ATPase activity and of fractional shortening was linear among the four groups. These studies demonstrate that physiologic and pathologic hypertrophy in the rat have distinctly opposite effects on contractile proteins and contractile performance. When one type of hypertrophy is superimposed on the other the effects are additive.
D000199:Actins / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D003285:Contractile Proteins / Q000378:metabolism; D003326:Coronary Circulation; D005260:Female; D006978:Hypertension, Renovascular / Q000150:complications / Q000503:physiopathology*; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology; D009218:Myosins / Q000378:metabolism*; D005082:Physical Exertion; D051381:Rats; D013318:Stroke Volume; D013550:Swimming
D000199:Actins; D003285:Contractile Proteins; D007527:Isoenzymes; D000251:Adenosine Triphosphatases; D009218:Myosins; D000252:Calcium-Transporting ATPases