Pathophysiology of abnormalities involving calcium signalling during cardiac muscle contraction

Ram B. Singh, Manal M.A. Smail, Sunil Rupee, Khemraj Rupee, Keshore Bidasee, Ernest Adeghate, Adrian Isaza, Abla Ismail, Jaipaul Singh

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Each cardiac myocyte fires an action potential (AP) due to excitation propagated from the sinoatrial node to elicit cardiac muscle contraction by a mechanism, known as excitation–contraction coupling. Cardiac contractility is regulated by the changes in intracellular free Ca2+ [Ca2+]i concentration and physiological function requires that [Ca2+]i should be sufficiently high in systole and low in diastole. Ca2+ needed for contraction comes mainly from the sarcoplasmic reticulum (SR) and is released by the process of calcium-induced calcium release. The mechanisms that enhance [Ca2+]i increase the amount of ATP hydrolyzed and the force generated by the actin and myosin interactions, including the velocity of shortening. Physiologically, [Ca2+]i is influenced primarily by beta-adrenoceptor-coupled mechanisms. During the initiation of cardiac contraction, the cardiac dyad is a specialized signaling communication concerned primarily with the clusters of L-type Ca2+ channels (LTCCs) on the sarcolemma closely apposed (≈15nm) across the dyadic cleft to clusters of ryanodine receptors on the SR membrane. The cardiac dyad contains additional structures that may contribute to the modulation of Ca2+ release from the SR during systole. Extensively studies demonstrated that Na+-Ca2+-exchange, via its reverse-mode action, can contribute to Ca2+ influx early during the AP. As such, an increase in LTCCs may indicate that influx of Ca2+ is greater than efflux. This increases the amount of Ca2+ in the cell and SR until the resulting increase of the amplitude of the Ca2+ transient increases efflux to a level that restores flux balance. This review is related to the molecular changes occurring in cardiac calcium homeostasis in health and disease.

Original languageEnglish
Title of host publicationPathophysiology, Risk Factors, and Management of Chronic Heart Failure
PublisherElsevier
Pages149-158
Number of pages10
ISBN (Electronic)9780128229729
ISBN (Print)9780128231111
DOIs
Publication statusPublished - Jan 1 2024

Keywords

  • action potential
  • calcium
  • Cardiac muscle
  • excitation–contraction coupling
  • repolarization

ASJC Scopus subject areas

  • General Agricultural and Biological Sciences
  • General Biochemistry,Genetics and Molecular Biology

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