Cardiovascular Division, Harvard Thorndike Laboratory, Beth Israel Hospital, Harvard Medical School, Boston, MA, U.S.A.
Abstract:
Phasic release of calcium from the sarcoplasmic reticulum occurs in all mammalian cardiac preparations when the intracellular calcium concentration is sufficiently high. The phasic calcium release is often sufficient to trigger electrophysiological responses and aftercontractions. These can be detrimental to normal cardiac function. We induced phasic calcium release in ferret papillary muscles loaded with the calcium indicator aequorin. Development of phasic calcium release was associated with an increase in resting and peak Ca2+]i. Inhibiting sodium channels with yohimbine reduced resting Ca2+]i and prevented phasic calcium release. We propose a mechasism where by reduced Na+]i, and the subsequent increased efflux of calcium via sodium/calcium exchange reduced Ca2+]i.