1976
DOI: 10.1016/0002-9149(76)90428-8
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A metabolic control mechanism for calcium ion influx that may protect the ventricular myocardial cell

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Cited by 258 publications
(61 citation statements)
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“…An increased level of intracellular free calcium ions in the ischemic myocardial cells induces cellular damage (27) and increases the resistance of cell-to-cell electrical junctions (28)(29)(30). It has been reported that catecholamine-induced myocardial necrosis caused by excessive intracellular calcium accumulation was prevented by pretreatment with verapamil (31).…”
Section: Discussionmentioning
confidence: 99%
“…An increased level of intracellular free calcium ions in the ischemic myocardial cells induces cellular damage (27) and increases the resistance of cell-to-cell electrical junctions (28)(29)(30). It has been reported that catecholamine-induced myocardial necrosis caused by excessive intracellular calcium accumulation was prevented by pretreatment with verapamil (31).…”
Section: Discussionmentioning
confidence: 99%
“…(Note that only a small fraction of cyto-526 chrome c is bound to membranes (Cortese et al, 1998) after a lag-time of a few minutes in rat (Tremblay et al, 1991) and 544 human glomerulosa cells (Gallo-Payet et al, 1996). Similarly to 545 myocardiac cells (Sperelakis and Schneider, 1976) (Enyedi et al, 1985), followed by Ca 2+ influx (Hunyady 579 et al, 1994;Kramer, 1988 nists. In addition to G q angiotensin II also activates the adenylyl cy-590 clase inhibitory G protein G i (Enyedi et al, 1986;Maturana et al, 591 1999).…”
Section: à4mentioning
confidence: 99%
“…A number of possible mechanisms have been considered, including allosteric regulation of Ca2+ channel function (Plant, Standen & Ward, 1983), modulation of voltage-dependent inactivation by Ca2+ (Lee, Marban & Tsien, 1985), and activation of Ca2+-dependent phosphatases (Chad & Eckert, 1986). While this last hypothesis is supported by repeated suggestions that only phosphorylated Ca2+ channels are functional (Sperelakis & Schneider, 1976;Reuter & Scholz, 1977;Bean, Nowycky & Tsien, 1984; Armstrong & Eckert, 1987;Hymel, Striessnig, Glossmann & Schindler, 1988; Nunoki, Florio & Catterall, 1989), an absolute requirement for channel phosphorylation has been disputed vigorously (Kameyama, Hescheler, Hofmann Kameyama, Hescheler, Mieskes & Trautwein, 1986;Trautwein, Cavalie, Flockerzi, Hofmann & Pelzer, 1987). Furthermore, even if this point were conceded it would still leave open the question of whether a rise in [Ca2+]i promotes Ca2+ channel dephosphorylation (Byerly, Leung & Yazejian, 1988 (Hadiey & Lederer, 1991 a).…”
Section: Introductionmentioning
confidence: 99%