Journal
BIOPHYSICAL JOURNAL
Volume 78, Issue 1, Pages 334-343Publisher
CELL PRESS
DOI: 10.1016/S0006-3495(00)76596-9
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Funding
- NHLBI NIH HHS [HL30077, HL09412] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL030077, R01HL030077] Funding Source: NIH RePORTER
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Our aim was to measure the influence of sarcoplasmic reticulum (SR) calcium content ([Ca](SRT)) and free SR [Ca] ([Ca](SR)) on the fraction of SR calcium released during voltage clamp steps in isolated rabbit ventricular myocytes. [Ca](SRT), as measured by caffeine application, was progressively increased by conditioning pulses. Sodium was absent in both the intracellular and in the extracellular solutions to block sodium/calcium exchange. Total cytosolic calcium flux during the transient was inferred from I-Ca, [Ca](SRT), [Ca](i), and cellular buffering characteristics. Fluxes via the calcium current (I-Ca), the SR calcium pump, and passive leak from the SR were evaluated to determine SR calcium release flux (J(rel)), Excitation-contraction (EC) coupling was characterized with respect to both gain (integral J(rel)/ integral /(Ca) and fractional SR calcium release. Both parameters were virtually zero for a small, but measurable [Ca](SRT). Gain and fractional SR calcium release increased steeply and nonlinearly with both [Ca](SRT) and [Ca](SR). We conclude that potentiation of EC coupling can be correlated with both [Ca](SRT) and [Ca](SR). While fractional SR calcium release was not linearly dependent upon [Ca](SR), intra-SR calcium may play a crucial role in regulating the SR calcium release process.
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