A vibrating calcium (Ca2+)-selective electrode measured Ca2+ flux across the membrane of trabeculae from the ventricle of the marine gastropod, Busycon canaliculatum. Because the neuropeptide FMRFamide increases both systolic force and rate in the hearts of most mollusc species, the present experiments were conducted to study how Ca2+ may be mobilized by FMRFamide during excitation-contraction coupling (E-C coupling). Ca2+ efflux was consistently recorded from the trabeculae in response to FMRFamide. This efflux was the result of the sarcolemma redistributing Ca2+ into the extracellular compartment after a preceding rapid Ca2+ influx. Ca2+ efflux stimulated by FMRFamide was blocked by the L-type Ca2+ channel blocker verapamil. Conversely, diltiazem potentiated FMRFamide responses. Neither verapamil of diltiazem alone had any effect on spontaneous basal efflux. However, if FMRFamide was present, the membrane was responsive to the action of the Ca2+ channel blockers, suggesting that a use-dependent mechanism was involved. During spontaneous basal efflux, the Na-Ca exchanger was responsible for only 20% of the total Ca2+ efflux while during FMRFamide treatment the Na-Ca exchanger may have contributed about 60% to the total Ca2+ efflux. FMRFamide may not only alter ion channel activity but may also indirectly regulate Ca2+ extrusion mechanisms during cardioexcitation.
|Original language||English (US)|
|Number of pages||8|
|Journal||Comparative Biochemistry and Physiology - A Physiology|
|State||Published - Feb 1997|
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