title: [Changes in myosin isoenzymes composition and the maximum shortening velocity in hypertrophic left ventricular muscle of rats].
abstract: Changes in unloaded maximum shortening velocity (Vmax) and myosin isoenzymes (MI) composition of rat left ventricular muscle were examined in the 8-week or 16-week Goldblatt hypertensive (H8, H16) and hypertension-regressive rats (R8). The Vmax was estimated by extrapolation to zero afterload from the tension-velocity curve of left ventricular papillary muscle, while the MI composition (V1, V2 and V3) was separated by polyacrylamide gel electrophoresis and determined by densitometry. The results showed that: (1) A slow age-dependent shift to V3 and a decrease in Vmax were observed in 16- and 24-week-old rats (S8, S16), in which V1/V3 ratio was decreased respectively by 38.9% and 61.0% and Vmax was decreased respectively by 8.3% and 13.3% when compared with that of the 8-week-old rats (S0). (2) There was a significant decrease in V1/V3 ratio and Vmax in 8-week (H8) and 16-week (H16) hypertension induced hypertrophic left ventricular muscle as evidenced by the fact that the V1/V3 ratio decreased by 84.4% and 93.5% and Vmax decreased by 33.3% and 48.3% in H8 and H16 as compared with that of the control rats (S0). (3) There was a partial recovery in Vmax and V1/V3 ratio in (R8) group rats. (4) The Vmax was positively correlated with the level of V1 (r = 0.9215, P < 0.01) and negatively with the level of V3 (r = 0.9071, P < 0.01) as analyzed in all the six experimental groups of a total of 48 rats (S0, S8, S16, H8, H16, R8). In conclusion, a significant shift of the myosin isoenzymes towards low ATPase activity V3 might be the biochemical mechanism responsible, at least in part, for the decrease in maximum shortening velocity in the hypertrophic left ventricular muscle induced by pressure overload.
authors.affiliation: Laboratory of Cardiovascular Physiology, Human Medical University, Changsha.
authors.forename: L Q
authors.initials: LQ
authors.lastname: Liu
authors.forename: Y X
authors.initials: YX
authors.lastname: Li
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000473:pathology*; D006973:Hypertension / Q000378:metabolism; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D018995:Myosin Heavy Chains / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D010210:Papillary Muscles / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013718:Tensile Strength
chemical_list: D007527:Isoenzymes; D018995:Myosin Heavy Chains; D009218:Myosins