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Simulated calcium current can both cause calcium loading in and trigger calcium release from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell

By Alexandre Fabiato


ABSTRACT Skinned canine cardiac Purkinje cells were stimulated by regularly repeated microinjection-aspiration sequences that were programmed to simulate the fast initial component of the transsarcolemmal Ca 21 current and the subsequent slow component corresponding to noninactivating Ca21 channels. The simulated fast component triggered a tension transient through Ca 2+-induced release of Ca 21 from the sarcoplasmic reticulum (SR). The simulated slow component did not affect the tension transient during which it was first introduced but it potentiated the subsequent transients. The potentiation was not observed when the SR function had been destroyed by detergent. The potentiation decreased progressively when the slow component was separated by an increasing time interval from the fast component. The potentiation was progressive over several beats under conditions that decreased the rate of Ca" accumulation into the SR (deletion of calmodulin from the solutions; a decrease of the temperature from 22 to 12°C). In the presence of a slow component, an increase of frequency caused a positive staircase, and the introduction of an extrasystole caused a postextrasystolic potentiation. There was a negative staircase and no postextrasystolic potentiation in the absence of a slow component. These results can be explained by a time- and Ca2'-dependent functional separation of the release and accumulation processes of the SR, rather than by Ca21 circulation between anatomically distinct loading and release compartments. The fast initial component of transsarcolemmal Ca21 current would trigger Ca 2 ' release, whereas the slow component would load the SR with an amount of Ca2 ' available for release during the subsequent tension transients. Downloaded from jgp.rupress.org on February 22, 201

Year: 1985
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