Abstract
Rats with isoproterenol-induced cardiomegaly were evaluated for myocardial actomyosin and total protein content (mg/g tissue), hemodynamic changes and actomyosin adenosine triphosphatase (ATPase) activity. Maximum increase in heart mass (50.8%) was seen after 14 consecutive days of isoproterenol injection (5.25 mg/kg). Changes in heart size were determined by comparison of dry ventricle weights of treated and control animals; heart weight: final body weight ratios were not used to evaluate cardiomegaly since it was observed that the isoproterenol-injected animals gained less weight than control animals. The enlarged hearts of the treated animals had a normal total protein content (mg/g tissue) but actomyosin content was decreased by 8.6% ( P < 0.02). Doses of nitroglycerin which produced hypotension comparable to that of isoproterenol did not result in increases in cardiac mass. It was concluded that the primary stimulus for isoproterenol-induced cardiomegaly was related to its direct effect on the heart rather than its hypotensive effect. Actomyosin ATPase activity was evaluated using indirect (superprecipitation and turbidity changes) and direct measurements (inorganic phosphate release). Direct and indirect measurements of ATP hydrolysis, under varying conditions (changes in [Mg 2+], protein concentration, and aging of actomyosin) revealed that cardiac actomyosin from chronically treated animals (14 days) had a significantly lower ATPase activity. The same animals exhibited a significantly decreased heart rate (22%; P < 0.01). These animals also showed a trend toward decreased pulse pressure and mean blood pressure. The decrease in heart rate was of the same magnitude as the average decrease in actomyosin ATPase activity (21%). The reduced ATPase activity of actomyosin in the enlarged hearts may account for the slower heart rate in these animals; however, other factors influencing heart rate have not been excluded.
Published Version
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