Biochemistry (Moscow)

, Volume 77, Issue 11, pp 1248–1257

Redox control of cardiac rhythm

Authors

    • Russian Cardiological Research and Production Complex
Review

DOI: 10.1134/S000629791211003X

Cite this article as:
Kapelko, V.I. Biochemistry Moscow (2012) 77: 1248. doi:10.1134/S000629791211003X

Abstract

The rhythm of cardiac beats is generated by pacemaker cells differing from other cardiomyocytes by the presence of slow diastolic depolarization. Consistently activated transmembrane ionic currents provide cyclic excitation of pacemakers, forming the original “membrane clocks”. A new concept has been forwarded in the last decade according to which periodic fluctuations in myoplasmic Ca2+ level (“calcium clocks”) not only influence a course of “membrane clocks”, but they also can serve as independent generators of the rhythm. Transport of Ca2+ in cells is under constant influence of active forms of oxygen and nitrogen. Both superoxide and NO in moderate doses facilitate Ca2+ output from the sarcoplasmic reticulum, accelerating the course of “calcium clocks”, but in higher doses they have opposite effect that may be neutralized mainly by reduced glutathione. The control of cardiac rhythm by active forms of oxygen and nitrogen represents a feedback mechanism by which mitochondria and NO-synthases support Ca2+ homeostasis in cells that can be temporarily disturbed under mechanical loads or hypoxia.

Key words

diastolic depolarization Ca2+ transport ryanodine receptor sarcoplasmic reticulum mitochondria NO-synthases

Abbreviations

ETC

electron transport chain

GSNO

S-nitrosoglutathione

GSNOR

S-nitrosoglutathione reductase

NCX

sarcolemmal Na+/Ca2+-exchange mechanism

NOS

NO-synthase

ROS

reactive oxygen species

RyR

ryanodine receptor

Copyright information

© Pleiades Publishing, Ltd. 2012