Calcium signaling in cardiac muscle

K. M. Dibb*, A. W. Trafford, D. A. Eisner

*Corresponding author for this work

    Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

    Abstract

    The purpose of this chapter is to provide an overview of aspects of the state of knowledge of calcium signaling. Changes of the amplitude of the calcium transient are the major factor controlling the force of contraction of the heart during, for example, exercise. Abnormalities in calcium signaling have been implicated in clinically important conditions such as heart failure and cardiac arrhythmias. This chapter considers three ways in which the amount of calcium released from the SR by Calcium-Induced Calcium Release (CICR) can be increased: an increase of the trigger produced by the L-type calcium current and therefore the trigger for calcium release from the SR; an increase in the opening of the RyR such that more calcium is released for a given trigger L-type current and SR calcium content; and an increase of SR calcium content. The general area of calcium handling in heart failure is also reviewed extensively. Most studies find no change in the amplitude of the calcium current, and the most commonly accepted explanation of the decreased calcium transient is that it results from a decrease of SR calcium content.

    Original languageEnglish
    Title of host publicationHandbook of Cell Signaling
    EditorsRalph A. Bradshaw, Edward A. Dennis
    PublisherElsevier BV
    Chapter128
    Pages1027-1030
    Number of pages4
    Volume2
    Edition2
    ISBN (Print)9780123741455
    DOIs
    Publication statusPublished - 1 Dec 2010

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