|5-Hydroxytryptamine stimulates net Ca2+ flux in the ventricular muscle of a mollusc (Busycon canaliculatum) during cardioexcitation|
Devlin, C.L. (2001). 5-Hydroxytryptamine stimulates net Ca2+ flux in the ventricular muscle of a mollusc (Busycon canaliculatum) during cardioexcitation. Biol. Bull. 200: 344-350
In: Biological Bulletin. Marine Biological Laboratory: Lancaster, Pa. etc.. ISSN 0006-3185, more
Noninvasive, self-referencing calcium (Ca2+ ) electrodes were used to study the mechanisms by which 5-hydroxytryptamine (5-HT) affects net Ca2+ flux across the sarcolemma of myocytes from ventricular trabeculae (from a marine gastropod, Busycon canaliculatum). Treat-ment of isolated trabeculae with 5-HT causes a net Ca2+ efflux, which is 30% blocked by verapamil. These findings suggest that the efflux is in part the result of a previous Ca2+ influx through L-type Ca2+ channels and is due to a rapid Ca2+ extrusion mechanism inherent to the sarcolemma of these myocytes. 5-HT-induced net Ca2+ efflux is also reduced by about 40% by treatment with a sodium (Na 1 )-free, lithium (Li 1 )-substituted saline, which shuts down the Na-Ca exchanger during Ca2+ extrusion. Cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ ATPase, almost completely abolishes the 5-HT-in-duced net Ca2+ efflux, suggesting that the SR rather than the extracellular pool is the primary Ca2+ reservoir serving 5-HT-induced excitation.