Abstract
CATECHOLAMINES activate the enzyme, adenyl cyclase, which forms cyclic adenosine 3′,5′-monophosphate (3′,5′-AMP) in a variety of animal tissues1. This reaction system has been thought to control several metabolic processes, including glycogenolysis, steroidogenesis, keto-genesis, lipolysis and antidiuresis1–8. The positive ino-tropic and chronotropic effects of catecholamines on the heart are generally attributed to catechol interaction with the beta adrenergic receptor site. Rall and Sutherland2 and Mayer et al.9 have proposed that 3′, 5′-AMP might directly affect cardiac beta receptors by mediating hormone-induced changes in contractile force without necessarily involving glycogenolysis. During the course of investigations in the isolated perfused rat liver, 3′,5′-AMP was observed to induce delayed vasomotor changes unrelated to its glycogenolytic action10. This suggested that 3′, 5′-AMP might have a direct vascular effect on smooth muscle. Although 3′,5′-AMP produces hypergly-caemia in intact animals1,10–13, correlation of its metabolic action with possible regulation of cardiac activity has not been previously investigated.
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LEVINE, R., VOGEL, J. Cardiovascular and Metabolic Effects of Adenosine 3′,5′-Monophosphate in vivo. Nature 207, 987–988 (1965). https://doi.org/10.1038/207987a0
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DOI: https://doi.org/10.1038/207987a0
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