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Activators of sodium, calcium and potassium channels modulate the cardiac effects of Quinidine in vitro

Activators of sodium, calcium and potassium channels modulate the cardiac effects of Quinidine in vitro

Pharmacology and Toxicology 77(5): 346-351

Quinidine (25.5 mu-mol/l) reduced the beating frequency of isolated right guinea-pig atria, caused a negative inotropic effect in papillary muscles and slightly raised the contractile force of left atria. The functional refractory period of both tissues was prolonged. A 20% increase of the extracellular sodium concentration did not reverse the effects of quinidine. The Na-channel activator BDF 9148 (1 mu-mol/l) and the Ca-channel agonist Bay-K-8644 (0.5 mu-mol/l) further increased the contractile force and caused an additional prolongation of the functional refractory period in quinidine-pretreated atria. Only Bay-K-8644 was able to reverse the negative inotropic effect of quinidine in papillary muscles. The influence of Bay-K-8644 on the contractile force in quinidine-pretreated muscles was not attenuated by lemacalim (3 mu-mol/l), an activator of ATP-dependent potassium channels, but the duration of the functional refractory period was significantly reduced. These results suggest that a combination of a calcium channel activator and a potassium channel opener might be able to improve the treatment of quinidine intoxications.

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Accession: 008102749

Download citation: RISBibTeXText

PMID: 8778748

DOI: 10.1111/j.1600-0773.1995.tb01039.x

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