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Journal of Experimental Biology, Vol 179, Issue 1 47-61, Copyright © 1993 by Company of Biologists

JOURNAL ARTICLES

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

C. L. Devlin

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.

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