An Analysis of Control of the Ventricle of the Mollusc Mercenaria Mercenaria Ii. Ionic Mechanisms Involved in Excitation by 5-hydroxytryptamine

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 (Cl2) 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 10210 mol l–1, to 1026 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 5HT higher than 1025 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 9–18mmol l21. 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 1026 mol l–1 5-HT; nor did the removal of Cl2 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.