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Endocrinology Vol. 138, No. 12 5161-5169
Copyright © 1997 by The Endocrine Society

ARTICLES

Consequences of Growth Hormone Deficiency on Cardiac Structure, Function, and ß-Adrenergic Pathway: Studies in Mutant Dwarf Rats1

Antonio Cittadini, Hinrik Strömer, Dorothy E. Vatner, Jessica D. Grossman, Sarah E. Katz, Ross Clark, James P. Morgan and Pamela S. Douglas

Charles A. Dana Research Institute and the Harvard-Thorndike Laboratory, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School (A.C., H.S., J.D.G., S.E.K., J.P.M., P.S.D.), Boston, Massachusetts 02215; New England Regional Primate Research Center (D.E.V.), Southborough, Massachusetts 01772; and Genentech (R.C.), South San Francisco, California 94080

Address all correspondence and requests for reprints to: Pamela S. Douglas, M.D., Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215. E-mail: pdouglas{at}bidmc.harvard.edu

To evaluate GH’s role in cardiac physiology and its interrelationship with the ß-adrenergic system, we studied GH-deficient dwarf (dw/dw) and control rats in 4 groups of 20 each: dwarf group receiving placebo, dwarf-GH group receiving 2 mg/kg GH, dwarf-GH-propranolol group receiving 2 mg/kg GH and 750 mg/liter propranolol, and a control group of Lewis rats receiving placebo. Dwarf rats showed reduced left ventricular weight and myocyte cross-sectional area, and impaired cardiac performance in vitro. Left ventricular pressure-volume curves showed a shift upward and leftward, indicating reduced distensibility. These abnormalities reversed after GH treatment regardless of concomitant propranolol administration. Although isoproterenolol responsiveness was reduced in dwarf rats, there were no differences in ß-adrenergic receptor density, affinity, Na+,K+-adenosine triphosphatase activity, or adenylyl cyclase activity.

In summary, myocyte size, cardiac structure, myocardial contractility, and distensibility are abnormal in GH deficiency. The effects of GH are not mediated by the ß-adrenergic pathway, which, in turn, is unaffected by changes in the GH-insulin-like growth factor I axis. Thus, GH plays a regulatory role in normal cardiac physiology that is independent of the ß-adrenergic system.




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