STEPHEN E. EPSTEIN, M.D.; C. LYNN SKELTON, M.D.; GERALD S. LEVEY, M.D.; MARK ENTMAN, M.D.
The activity of many hormones can be related to their capacity to increase adenyl cyclase activity in their target organs. Evidence that the augmentation of myocardial contractility produced by catecholamines is mediated by adenyl cyclase activation is summarized. Glucagon and thyroid hormone also enhance myocardial adenyl cyclase activity, findings compatible with the hypothesis that activation of this enzyme may also be responsible for the increased contractility produced by glucagon and associated with hyperthyroidism. The inotropic action of epinephrine and glucagon may be due to an increase in sarcotubular calcium stores, an effect that appears to be related to activation of an adenyl cyclase in the microsomal fraction. Chronic cardiac decompensation did not alter the capacity of norepinephrine to enhance contractility or activate adenyl cyclase, but it markedly impaired the capacity of glucagon to elicit these responses. Thus, glucagon may have limited value in
the treatment of patients with chronic heart failure.
STEPHEN E. EPSTEIN, C. LYNN SKELTON, GERALD S. LEVEY, MARK ENTMAN. Adenyl Cyclase and Myocardial Contractility. Ann Intern Med. 1970;72:561–578. doi: 10.7326/0003-4819-72-4-561
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Published: Ann Intern Med. 1970;72(4):561-578.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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