DEATON, L.E.: Response of Bivalve Ventricles to 5HT and FMRFamide: Effects of Protein Kinase Inhibitors
Cardiac output in bivalves is controlled by the actions of neurotransmitters and neurohormones. These agents include 5-hydroxytryptamine (5HT), acetylcholine (Ach) and Phe-Met-Arg-Phe-NH2(FMRFamide). 5HT and FMRFamide are cardioexcitatory in some bivalve species and inhibitory in others. The cellular mechanisms that are involved in the effects of FMRFamide and 5HT on the bivalve heart are unclear. Both 5HT and FMRFamide have been shown to increase cAMP in bivalve ventricles, but forskolin, a protein kinase A agonist has no effect on bivalve cardiac muscle. Phorbol esters, potent protein kinase C agonists, have also been shown to excite bivalve ventricles. We challenged isolated ventricles of the mussel Geukensia demissa and the clam Mercenaria mercenaria with a variety of protein kinase A and C antagonists. In addition, the effects of the kinase blockers on the responses of the ventricles to 5HT and FMRFamide were tested. The kinase A inhibitor H-89 and the C kinase antagonists H-7, R59022, and staurosporine had no effect on the mechanical activity of either Mercenaria or Geukensia ventricles. Cholera toxin, a kinase A agonist, had no effect on the heart of either bivalve. The C kinase antagonist chelerythrine chloride excited Mercenaria but not Geukensia ventricles. None of the protein kinase agents tested blocked the response of the ventricles to 5HT or FMRFamide. These results suggest that the actions of pharmaceutical probes of second messenger activity in molluscs may not be similar to their actions in vertebrate systems. The details of the cellular mechanisms involved in the cardioregulatory actions of 5HT and FMRFamide in bivalves remain elusive.
