ABSTRACT
This study focuses on the ionic mechanisms involved in serotonergic control of the ventricle from the mollusc MercenariaMercenaria. 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 10−5mol l−1caused 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 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−15-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.
