Why, where, and when do cardiac myocytes express inositol 1,4,5-trisphosphate receptors?
Author(s) -
Martin D. Bootman,
H. Llewelyn Roderick
Publication year - 2007
Publication title -
american journal of physiology-heart and circulatory physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.524
H-Index - 197
eISSN - 1522-1539
pISSN - 0363-6135
DOI - 10.1152/ajpheart.01378.2007
Subject(s) - ryanodine receptor , sarcolemma , inositol , myocyte , biophysics , chemistry , endoplasmic reticulum , receptor , inositol trisphosphate , intracellular , depolarization , inositol trisphosphate receptor , microbiology and biotechnology , biochemistry , biology
The sequence of events leading to a Ca 2+ signal during cardiac excitation-contraction (EC) coupling is well known. With each beat, the propagating action potential depolarizes the sarcolemma of the excitable myocytes within the heart. Membrane depolarization leads to the activation of voltage-operated Ca 2+ channels (VOCs), thereby causing a brief influx of Ca 2+ . The Ca 2+ influx is sensed and amplified by Ca 2+ release channels known as ryanodine receptors (RyRs), which are expressed on the sarcoplasmic reticulum (SR) in close apposition to the VOCs. The RyRs are activated by the Ca 2+ permeating across the VOCs via a process known as Ca 2+ -induced Ca 2+ release (CICR).
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom