5-Hydroxytryptamine stimulates net Ca super(2+) flux in the ventricular muscle of a mollusc (Busycon canaliculatum) during cardioexcitation

Noninvasive, self-referencing calcium (Ca super(2+)) electrodes were used to study the mechanisms by which 5-hydroxytryptamine (5-HT) affects net Ca super(2+) flux across the sarcolemma of myocytes from ventricular trabeculae (from a marine gastropod, Busycon canaliculatum). Treatment of isolated trabeculae with 5-HT causes a net Ca super(2+) efflux, which is 30% blocked by verapamil. These findings suggest that the efflux is in part the result of a previous Ca super(2+) influx through L-type Ca super(2+) channels and is due to a rapid Ca super(2+) extrusion mechanism inherent to the sarcolemma of these myocytes. 5-HT-induced net Ca super(2+) efflux is also reduced by about 40% by treatment with a sodium (Na super(+))-free, lithium (Li super(+))-substituted saline, which shuts down the Na-Ca exchanger during Ca super(2+) extrusion. Cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca super(2+) ATPase, almost completely abolishes the 5-HT-induced net Ca super(2+) efflux, suggesting that the SR rather than the extracellular pool is the primary Ca super(2+) reservoir serving 5-HT-induced excitation.