PT  - JOURNAL ARTICLE
AU  - BETTY J WILLIAMS
AU  - STEVEN E MAYER
TI  - Hormonal Effects on Glycogen Metabolism in the Rat Heart <em>in Situ</em>
DP  - 1966 Sep 01
TA  - Molecular Pharmacology
PG  - 454--464
VI  - 2
IP  - 5
4099  - http://molpharm.aspetjournals.org/content/2/5/454.short
4100  - http://molpharm.aspetjournals.org/content/2/5/454.full
SO  - Mol Pharmacol1966 Sep 01; 2
AB  - Several hormones known to affect tissue glycogen concentration have been studied in the open-chested rat in relation to their effects on the enzymes of cardiac glycogen metabolism. Epinephrine, given by rapid intravenous injection, increased phosphorylase a activity and glucose-6-P concentration in both heart and skeletal muscle. In contrast, glycogen synthetase I activity was increased in heart and decreased in skeletal muscle. Continuous infusion of epinephrine (1 µg/kg min-1) caused marked glycogenolysis in skeletal muscle, but no change in heart glycogen concentration. In these experiments a transient increase was seen in cardiac glycogen synthetase I activity, while the percentage synthetase I decreased in skeletal muscle. Infusion of 2.5 µg/kg min-1 of epinephrine decreased cardiac glycogen and produced a biphasic change in synthetase I activity, consisting of first an increase, then a decrease in heart percentage of glycogen synthetase I. All these effects of epinephrine were prevented by prior administration of the beta adrenergic blocking agent pronethalol. Glucagon caused marked cardiac glycogenolysis, an increase in the percentage of phosphorylase a, but no change in the percentage of synthetase I. These effects were also antagonized by pronethalol pretreatment. Insulin caused an increase in the percentage of synthetase I in heart without affecting phosphorylase activity. The increase in synthetase I activity was unaffected by the administration of pronethalol. Thus, in heart as in skeletal muscle, hormones affect the critical steps in glycogen synthesis and degradation, perhaps in part through a common pathway sensitive to beta adrenergic blockade. However, other factors such as physiological changes in cardiac muscle may be involved in the magnitude and direction of the response. ACKNOWLEDGMENT The authors wish to thank Mrs. Margaret Maltbie for technical assistance and Dr. K. R. Hornbrook for his help in the preparation of the manuscript. This study was supported by a grant (HE 04626), a Career Development Award to S.E.M. (GM-6257) and Pharmacology Training Grant 2T1GM179-06 from the Public Health Service. This work was used to fulfill in part the requirements for the degree of Doctor of Philosophy (B.J.W.), at Emory University.