AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 275: H422-H430, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 2, H422-H430, August 1998

Cs+ inhibits spontaneous Ca2+ release from sarcoplasmic reticulum of skinned cardiac myocytes

Makoto Kawai, Munir Hussain, and Clive H. Orchard

Department of Physiology, University of Leeds, Leeds LS2 9NQ, United Kingdom

The effect of Cs+ on the function of the cardiac sarcoplasmic reticulum (SR) has been investigated in skinned cardiac myocytes. Isolated rat ventricular myocytes were permeabilized using saponin and then perfused with a solution containing 150 nmol/l Ca2+ and 10 µmol/l fura 2. Fura 2 fluorescence from the skinned cell was monitored to assess SR Ca2+ release. The frequency of spontaneous Ca2+ release from the SR decreased when K+ in the bathing solution was completely replaced with Cs+. Cs+ had little effect on the amplitude of spontaneous release but prolonged both the rise time and decay time. The SR Ca2+ content, assessed by application of caffeine, was reduced in the Cs+ solution. Cyclopiazonic acid produced effects similar to those of Cs+. Extracellular Cs+ (20 mmol/l) increased the amplitude of the Ca2+ transient and the SR Ca2+ content in intact field-stimulated cells but had little effect on the Ca2+ transient when the amplitude and duration of depolarization were kept constant using voltage clamp. These data suggest that Cs+ slows Ca2+ movement across the SR membrane, possibly by blocking the SR K+ channel, but has additional effects in intact cells that overcome its inhibitory effects on the SR.

cesium; cardiac sarcoplasmic reticulum potassium channel; counterion; cyclopiazonic acid; voltage clamp


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