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Regulation of Calcium Slow Channels in Cardiac Muscle and Vascular Smooth Muscle Cells

  • Nicholas Sperelakis
  • Noritsugu Tohse
  • Yusuke Ohya
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 311)

Abstract

Considerable attention during the past few years has been given to phosphorylation of ion channels as a means whereby the activity of the ion channels can be regulated. This article will cover the evidence that cyclic nucleotides regulate the Ca2+ influx into the myocardial cells during each cardiac cycle and into vascular smooth muscle (VSM) cells. This regulation is presumable mediated by phosphorylation(s) of the Ca2+ slow channel protein and/or of associated regulatory protein(s). In myocardial cells, such phosphorylation (Fig. 1) presumably (a) increases the number of Ca2+ slow channels available for voltage activation during the action potential (AP); (b) increases the probability of their opening, and (c) increases their mean open time. A greater density of available Ca2+ channels increases Ca2+ influx and inward Ca2+ slow current (Isi) during the AP, and so increases the force of contraction of the heart. In some VSM cells, phosphorylation by cAMP-PK or cGMP-PK inhibits the Ca2+ slow channel activity and thereby produces vasodilation, whereas phosphorylation by PK-C stimulates the Ca2+ slow channel activity and produces vasoconstriction.

Keywords

Atrial Natriuretic Peptide Phorbol Ester Cyclic Nucleotide Slow Channel Positive Inotropic Agent 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1992

Authors and Affiliations

  • Nicholas Sperelakis
    • 1
  • Noritsugu Tohse
    • 1
  • Yusuke Ohya
    • 1
  1. 1.Department of Physiology and BiophysicsUniversity of Cincinnati, College of MedicineUSA

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