Inotropic agents modulate gap junctional conductance between cardiac myocytes

Janis M Burt, D. C. Spray

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129 Citations (Scopus)

Abstract

Cardiac gap junction channels mediate the intercellular exchange of second messenger and small molecules. Through effects on conduction velocity, enhanced junctional conductance (g(j)) facilitates rapid and synchronous activation of the contractile myocardium, whereas reduced g(j) slows activation and could contribute to arrhythmogenesis. We report here that g(j) is enhanced by agents that elevate intracellular adenosine 3',5'-cyclic monophosphate (cAMP; 8-bromo-cAMP or isoproterenol) and is depressed by agents that elevate intracellular guanosine, 3',5'-cyclic monophosphate (cGMP; 8-bromo-cGMP or carbachol). Both effects occur with a time course comparable to the inotropic events mediated by these agents. The effect of cAMP on g(j) is not dependent on simultaneous changes in intracellular calcium; however, during calcium-overload conditions cAMP can precipitate calcium-dependent uncoupling. These results indicate that cyclic nucleotide-dependent changes in g(j) may contribute to the inotropic effects of these agents. Furthermore, the results suggest that the inotropic effect of cAMP includes a calcium-independent component.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume254
Issue number6
StatePublished - 1988

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Cardiac Myocytes
Calcium
8-Bromo Cyclic Adenosine Monophosphate
Gap Junctions
Cyclic Nucleotides
Cyclic GMP
Carbachol
Second Messenger Systems
Isoproterenol
Cyclic AMP
Myocardium

ASJC Scopus subject areas

  • Physiology

Cite this

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AU - Spray, D. C.

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