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AJP - Heart and Circulatory Physiology, Vol 259, Issue 1 264-H267, Copyright © 1990 by American Physiological Society
ARTICLES |
S. Pelzer, Y. M. Shuba, T. Asai, J. Codina, L. Birnbaumer, T. F. McDonald and D. Pelzer
II. Physiologisches Institut, Medizinische Fakultat Universitat des Saarlandes, Homburg/Saar, Federal Republic of Germany.
A severalfold increase in calcium current (ICa) is a signal feature of the maximal beta-adrenergic response of the heart. It is generally ascribed to enhanced adenosine 3',5'-cyclic monophosphate (cAMP)-dependent phosphorylation of calcium (Ca) channels after beta-receptor activation of the guanosine nucleotide-binding (G) protein Gs, and Gs activation of the adenylyl cyclase cascade. We blocked phosphorylation pathways in guinea pig cardiomyocytes to unmask other possible ICa-stimulatory modes. In blocked cells, ICa increased by approximately 50% during 1) beta-receptor activation of Gs, 2) intracellular activation of Gs, and 3) intracellular application of preactivated Gs, We conclude that fast, membrane-delimited Gs modulation participates in the physiological regulation of cardiac ICa.
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