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Excitation–Contraction Coupling In Skeletal Muscle: Comparisons With Cardiac Muscle
Author(s) -
Lamb Gd
Publication year - 2000
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2000.03224.x
Subject(s) - ryr1 , ryanodine receptor , skeletal muscle , muscle contraction , contraction (grammar) , biophysics , cardiac muscle , endoplasmic reticulum , chemistry , stimulation , myocyte , dihydropyridine , voltage dependent calcium channel , medicine , excitation–contraction coupling , ryanodine receptor 2 , calcium , endocrinology , biology , biochemistry
SUMMARY 1. The present review describes the mechanisms involved in controlling Ca 2+ release from the sarcoplasmic reticulum (SR) of skeletal muscle, which ultimately regulates contraction. 2. Comparisons are made between cardiac and skeletal muscle with respect to: (i) the role of the dihydropyridine receptors (DHPR) as Ca 2+ channels and voltage‐sensors; (ii) the regulation of the ryanodine receptor (RyR)/Ca 2+ ‐release channels in the SR; and (iii) the importance of Ca 2+ ‐induced Ca 2+ release. 3. It is shown that the key differences of the skeletal muscle Ca 2+ ‐release channel (RyR1), namely the increase in its stimulation by ATP and its inhibition by Mg 2+ , are critical for its direct regulation by the associated DHPR and, consequently, for the fast, accurate control of skeletal muscle contraction.