AN ANALYSIS OF CONTROL OF THE VENTRICLE OF THE MOLLUSC MERCENARIA MERCENARIA

Abstract

During spontaneous beating (autorhythmicity) in the bivalve ventricle, the cardiac action potential (AP) was generated by calcium (Ca2+) and sodium (Na+) influx. The initial fast rising phase (the ‘spike’) of the cardiac AP was dependent on extracellular Ca2+ concentration, whereas the slow plateau phase was Na+-dependent. The initial fast rising phase of the cardiac AP was abolished by treatment with a Ca2+-free saline or inorganic Ca2+ entry blockers, such as lanthanum chloride or cobalt. Conversely, this fast rising phase of the AP was potentiated by treatment with barium ions, the dihydropyridine-sensitive Ca2+ channel agonist Bay K 8644 or, unexpectedly, by the organic Ca2+ entry blocker diltiazem. The force of systolic beating was directly proportional to the amplitude of the fast rising phase of the cardiac AP. The Ca2+-dependent, fast rising phase of the AP was modulated by the level of extracellular Na+. Both the amplitude of the fast rising phase of the AP and coupled systolic force were increased by progressive reduction of extracellular Na+ concentration. The slow plateau phase was abolished by treatment with a Na+-free saline and potentiated by the Na+ ionophore monensin. The size of the Na+-dependent plateau was modulated by the level of extracellular Ca2+. When extracellular Ca2+ was removed from the bathing saline, both the amplitude and duration of the plateau phase were increased. Conversely, restoring extracellular Ca2+ to physiological levels decreased the size of the Na+-dependent plateau. Autorhythmicity was dependent on the level of extracellular potassium. In the absence of K+, neither a Ca2+-dependent fast rising phase nor a Na+-dependent plateau phase was recorded.