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1 Division of Cardiology, Internal Medicine III, and 2 Clinical Pharmacology and Therapeutics, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan
In hearts, intracellular acidosis disturbs contractile performance by decreasing myofibrillar Ca2+ response, but contraction recovers at prolonged acidosis. We examined the mechanism and physiological implication of the contractile recovery during acidosis in rat ventricular myocytes. During the initial 4 min of acidosis, the twitch cell shortening decreased from 2.3 ± 0.3% of diastolic length to 0.2 ± 0.1% (means ± SE, P < 0.05, n = 14), but in nine of these cells, contractile function spontaneously recovered to 1.5 ± 0.3% at 10 min (P < 0.05 vs. that at 4 min). During the depression phase, both the diastolic intracellular Ca2+ concentration ([Ca2+]i) and Ca2+ transient (CaT) amplitude increased, and the twitch [Ca2+]i decline prolonged significantly (P < 0.05). In the cells that recovered, a further increase in CaT amplitude and a reacceleration of twitch [Ca2+]i decline were observed. The increase in diastolic [Ca2+]i was less extensive than the increase in the cells that did not recover (n = 5). Blockade of sarcoplasmic reticulum (SR) function by ryanodine (10 µM) and thapsigargin (1 µM) or a selective inhibitor of Ca2+-calmodulin kinase II, 2-[N- (2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methyl benzylamine (1 µM) completely abolished the reacceleration of twitch [Ca2+]i decline and almost eliminated the contractile recovery. We concluded that during prolonged acidosis, Ca2+-calmodulin kinase II-dependent reactivation of SR Ca2+ uptake could increase SR Ca2+ content and CaT amplitude. This recovery can compensate for the decreased myofibrillar Ca2+ response, but may also cause Ca2+ overload after returning to physiological pHi.
cardiac myocyte; intracellular pH; intracellular Ca2+ concentration; ATPase
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