This study focuses on the ionic mechanisms involved in serotonergic control of the ventricle from the mollusc Mercenaria mercenaria. The effects of calcium (Ca2+), sodium (Na+), potassium (K+), magnesium (Mg2+) and chloride (Cl-) ions on the action of 5-hydroxytryptamine (5-HT) were tested using a sucrose-gap technique. 5-HT increased the amplitude and frequency of the cardiac action potentials (APs) and coupled systolic force in a range of concentrations from the threshold, at 10–10 mol l-1, to 10-6 mol l-1. Low, physiological doses of 5-HT increased the rate of rise and amplitude of the fast rising phase of the AP, and hastened the process of repolarization. Doses of 5-HT higher than 10-5 mol l-1 caused systolic arrest. The action of 5-HT was highly dependent on the presence of physiological levels of extracellular Ca2+. It had a maximal effect on systolic activity in a calcium chloride concentration range of 9–18 mmol l-1. The activity of 5-HT was blocked by treatment with Ca2+-free saline, with inorganic Ca2+ blockers (lanthanum or cobalt) or with an organic Ca2+ entry blocker (verapamil). The effects of 5- HT were potentiated by treatment with barium ions (Ba2+), by a dihydropyridine-sensitive Ca2+ agonist, Bay K 8644, or by a vertebrate Ca2+ entry blocker, diltiazem. Removal of extracellular Na+ or treatment with a Na+ ionophore, monensin, did not significantly affect excitation by 10-6 mol l-1 5-HT; nor did the removal of Cl- or Mg2+. Unlike Ca2+, these three ions probably did not have a critical role during the excitatory action of 5-HT. The excitatory action of 5-HT was not significantly altered by treatment with K+-free saline. When the membrane was depolarized by high-K+ salines, however, 5-HT was unable to elicit any APs or systolic contractions, suggesting that its mechanism may involve voltage-sensitive channels.

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