Local control of excitation‐contraction coupling in rat heart cells.

W. G. Wier, T. M. Egan, J. R. López‐López, C. W. Balke

Research output: Contribution to journalArticlepeer-review

220 Scopus citations

Abstract

1. Cytosolic free calcium ion concentration ([Ca2+]i) and whole‐cell L‐type Ca2+ channel currents were measured during excitation‐contraction (E‐C) coupling in single voltage‐clamped rat cardiac ventricular cells. The measurements were used to compute the total cellular efflux of calcium ions through sarcoplasmic reticulum (SR) Ca2+ release channels (FSR,rel) and the influx of Ca2+ via L‐type Ca2+ channels (FICa). 2. FSR,rel was elicited by depolarizing voltage‐clamp pulses 200 ms in duration to membrane potentials from ‐30 to +80 mV. Over this range, peak FSR,rel had a bell‐shaped dependence on clamp pulse potential. In all cells, the ‘gain’ of the system, measured as the ratio, FSR,rel(max)/FICa(max), declined from about 16, at 0 mV, to much lower values as clamp pulse voltage was made progressively more positive. We named this phenomenon of change in gain as a function of membrane potential, ‘variable gain’. At clamp pulse potentials in the range ‐30 to 0 mV, the gain differed from cell to cell, being constant at about 16 in some cells, but decreasing from high values (approximately 65) at ‐20 mV in others. 3. At clamp pulse potentials at which Ca2+ influx (FICa) was maintained, FSR,rel also had a small maintained component. When macroscopic Ca2+ influx was brief (1‐2 ms, during ‘tails’ of FICa), FSR,rel rose rapidly to a peak after repolarization and then declined with a half‐time of about 9 ms (typically). 4. The rising phase of [Ca2+]i transients could be interrupted by stopping Ca2+ influx rapidly (by voltage clamp). We therefore termed this phenomenon ‘interrupted SR Ca2+ release’.(ABSTRACT TRUNCATED AT 250 WORDS)

Original languageEnglish
Pages (from-to)463-471
Number of pages9
JournalThe Journal of Physiology
Volume474
Issue number3
DOIs
StatePublished - Feb 1 1994

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