Hormonal Control of Cardiac Myosin Adenosine Triphosphatase in the Rat

Author:

Rovetto Michael J.1,Hjalmarson Åke C.1,Morgan Howard E.1,Barrett Michael J.1,Goldstein Richard A.1

Affiliation:

1. supported in part by U. S. Public Health Service Grant HE 11534 from the National Heart and Lung Institute and by a grant from the Pennsylvania Heart Association. Dr. Rovetto is a Postdoctoral Fellow of the National Institutes of Health.

Abstract

Cardiac function was impaired in hearts from hypophysectomized rats. Corresponding to the decrease in performance, myosin from the hearts of these rats exhibited a decreased Ca 2+ -activated ATPase activity. Myosin ATPase activated by K + or NH 4 + was not different in any of the preparations studied. The decreased Ca 2+ -activated ATPase was observed in cardiac myosin but not in red or white skeletal muscle myosin. Treatment with thyroxine, but not with growth hormone, restored cardiac myosin ATPase and performance to normal. Hypothyroidism produced a decrease in cardiac myosin ATPase activity comparable to that seen after hypophysectomy, suggesting that the absence of thyroid hormone was responsible for the alterations. However, hyperthyroidism did not increase ATPase activity above normal values. Adrenalectomy failed to alter myosin ATPase. Anion exchange chromatography of the myosins and addition of various concentrations of Na + , Ca 2+ , and Mg 2+ did not abolish the differences in myosin ATPase. The results strongly suggest that the lower myosin ATPase activity in the absence of thyroid hormone was the result of a change in the myosin molecule per se and that the lower enzymatic activity was involved in the lower cardiac performance in these rats.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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