Isomyosin transitions in ventricles of aldosterone-salt hypertensive rats.

Abstract

The isomyosin composition in left and right ventricles from aldosterone-salt-treated hypertensive rats and from vehicle-infused and aldosterone-infused normotensive control rats was compared. A significant incremental increase (20%) in the percentage of V3 isomyosin and parallel decrease in the percentage of V1 isomyosin occurred in both left and right ventricles from aldosterone-salt-treated animals compared with those in normotensive vehicle-infused controls. No change in the ventricular isomyosin distribution was observed in animals infused with aldosterone without salt, which indicates that aldosterone does not directly affect the ventricular isomyosin composition. The changes in left ventricular isomyosin composition were accompanied by significant left ventricular hypertrophy (38%; p less than 0.05), whereas no hypertrophy was observed in the right ventricle. Plasma thyroxine levels were significantly lower in aldosterone-salt-treated rats (3.7 +/- 0.6 micrograms/dl; p less than 0.05) than in normotensive vehicle-infused (6.0 +/- 0.7 micrograms/dl) or aldosterone-infused (6.7 +/- 0.3 micrograms/dl) controls. These results indicate that factors such as alterations in thyroid status or a volume overload component of this hypertensive model, in addition to increased systolic blood pressure, may contribute to a biventricular shift in isomyosin composition in the aldosterone-salt model of hypertension.

Recovery after Cardioplegia in the Hypertrophic Rat Heart

“…The relative amounts of V 1 , V 2 , and V 3 isomyosins, expressed as percentages, were calculated from the area under each isomyosin transmittance peak. LV V 2 isomyosin content was divided equally between V 1 and V 3 so that total %V 3 ϭ %V 3 ϩ 0.5 (%V 2 ) [27]. Most gels were scanned two to four times and results were averaged for each gel.…”

“…V 3 exhibits the highest and V 1 the lowest efficiency of force generation [20,25]. V 1 predominates in the normal adult rat ventricle [26], but the fetal isoform V 3 is increased in hypertrophy due to hemodynamic overload [2,16,26,27]. Thyrotoxicosis, in contrast, causes hypertrophy with a predominance of V 1 [16,23], while thyroid insufficiency induces cardiac atrophy with increased V 3 [16,20].…”