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- W2011772600 abstract "Excitation–contraction coupling (ECC) in cardiac myocytes describes all events linking stimulation of the cell by the propagating electrical signal, to the eventual mechanical activity. In its narrow sense, however, ECC often refers to the mechanisms that underlie the transient rise in cytosolic [Ca2+], [Ca2+]i, which is a key element in these events. In skeletal muscle, contraction can continue in the absence of external Ca2+ (e.g. [ [1] Frank G.B Utilization of bound calcium in the action of caffeine and certain multivalent cations on skeletal muscle. J Physiol (Lond). 1962; 163: 254-268 Google Scholar ]), and it was proposed that the activator Ca2+ was derived from an internal store, the sarcoplasmic reticulum (SR). For long, cardiac muscle was regarded as similar to skeletal muscle, despite the fact that Ringer in 1883 had already shown that the frog heart stops beating in the absence of Ca2+ in the bathing medium. Morad and Goldman summarized the available data on cardiac muscle in 1973 [ [2] Morad M Goldman Y Excitation contraction in heart muscle: membrane control and development of tension. Prog Biophys Mol Biol. 1973; 27: 257-313 Crossref Scopus (207) Google Scholar ], leading to the working hypothesis that in cardiac muscle, both Ca2+ influx via the ‘slow current' during the action potential and triggered release from the SR contributed to the activator Ca2+, though the nature of this trigger was not clearly formulated. In the following years, Fabiato and Fabiato published landmark studies in skinned single cardiac cells, which indicated that Ca2+ entry via the Ca2+ current could act as the trigger for Ca2+ release from the SR, as well as loading the SR Ca2+ store (e.g. [ 3 Fabiato A Fabiato F Contractions induced by calcium-triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells. J Pharmacol Exp Ther. 1975; 249: 469-495 Google Scholar , 4 Fabiato A Time and calcium dependence of activation and inactivation of calcium-induced release of calcium from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell. J Gen Physiol. 1985; 85: 247-289 Crossref PubMed Scopus (681) Google Scholar , 5 Fabiato A Simulated calcium current can both cause calcium loading in and trigger calcium release from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell. J Gen Physiol. 1985; 85: 291-320 Crossref PubMed Scopus (343) Google Scholar ]). Theirs and other observations led to the proposal that in cardiac muscle, Ca2+ influx, not voltage per se, was the trigger for SR Ca2+ release, the Ca2+-induced Ca2+ release (CICR) vs. the charge-coupled Ca2+ release (CCCR) of skeletal muscle (reviewed in [ [6] Fabiato A Appraisal of the physiological relevance of two hypotheses for the mechanism of calcium release from the mammalian cardiac sarcoplasmic reticulum: calcium-induced release versus charge-coupled release. Mol Cell Biochem. 1989; 2: 135-140 Google Scholar ]). With the development of the patch clamp technique [ [7] Hamill O.P Marty A Neher E Sakmann B Sigworth F Improved patch-clamp techniques for high-resolution current recording from cell and cell-free membrane patches. Pflügers Arch. 1981; 391: 85-100 Crossref PubMed Scopus (15085) Google Scholar ], this hypothesis was tested in several sophisticated experiments in single intact cardiac myocytes, measuring membrane currents, [Ca2+]i, and contraction. The results strongly supported the CICR hypothesis and pointed towards the L-type Ca2+ current as the source of trigger Ca2+. Critical observations included: the bell-shaped voltage dependence of [Ca2+]i transients, the presence of Ca2+ release on repolarization from a strong depolarizing pulse, which did not induce a [Ca2+]i transient by itself (e.g. [ 8 Cannell M.B Berlin J.R Lederer W.J Effect of membrane potential changes on the calcium transient of single rat cardiac muscle cells. Science. 1987; 238: 1419-1423 Crossref PubMed Scopus (239) Google Scholar , 9 Beuckelmann D.J Wier W.G Mechanism of release of calcium from sarcoplasmic reticulum of guinea-pig cardiac cells. J Physiol (Lond). 1988; 405: 233-255 Google Scholar , 10 Callewaert G Cleemann L Morad M Epinephrine enhances Ca2+-current regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes. Proc Natl Acad Sci USA. 1988; 85: 2009-2013 Crossref PubMed Scopus (95) Google Scholar , 11 duBell W.H Houser S.R Voltage and beat dependence of Ca2+ transient in feline ventricular myocytes. Am J Physiol. 1989; 257: H746-759 PubMed Google Scholar ]), the lack of Ca2+ release when current through the L-type Ca2+ channel was carried by other ions [ [12] Nabauer M Callewaert G Cleemann L Morad M Regulation of calcium release is gated by calcium current, not gating charge, in cardiac myocytes. Science. 1989; 244: 800-803 Crossref PubMed Scopus (336) Google Scholar ], the dependence of CICR on the cardiac isoform of the Ca2+ channel [ 13 Tanabe T Mikami A Numa S Beam K.G Cardiac-type excitation–contraction coupling in dysgenic skeletal muscle injected with cardiac dihydropyridine receptor cDNA. Nature. 1990; 344: 451-453 Crossref PubMed Scopus (191) Google Scholar , 14 Tanabe T Beam K.G Adams B.A Niidome T Numa S Regions of the skeletal muscle dihydropyridine receptor critical for excitation–contraction coupling. Nature. 1990; 346: 567-569 Crossref PubMed Scopus (487) Google Scholar ], and the lack of an effect of voltage on CICR induced by flash photolysis [ [15] Niggli E Lederer W.J Voltage-independent calcium release in heart muscle. Science. 1990; 250: 565-568 Crossref PubMed Scopus (141) Google Scholar ]. Thus, by the early 1990s, the hypothesis that in cardiac muscle L-type Ca2+ current triggered SR Ca2+ release was generally accepted, and research focused on the mechanisms of this interaction." @default.
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- W2011772600 title "Triggering controversy in cardiac excitation–contraction coupling" @default.
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