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The action of procainamide and quinidine on the alpha 1-receptor-operated channels in smooth muscle cells of guinea-pig taenia caeci

The action of procainamide and quinidine on the alpha 1-receptor-operated channels in smooth muscle cells of guinea-pig taenia caeci

European Journal of Pharmacology 137(2-3): 233-240

The effect of procainamide (2.0-5.0 mM) and quinidine (0.2-1.0 mM) on the .alpha.1 response evoked by adrenaline (3 .times. 10-6 M) in smooth muscle cells of guinea-pig taenia caeci (22.degree. C) was studied in the presence of yohimbine (3 .times. 10-6 M), propranolol (3 .times. 10-6 M) or atropine (10-6 M). The electrotonic potential elicited by the application of a constant current to the preparation was slightly increased (about 10%) by procainamide (5.0 mM) but not by quinidine (1.0 mM). The double-sucrose gap method was used for measurements. The .alpha.1 response evoked by adrenaline in the absence of extracellular calcium (15 min) was represented by a transient hyperpolarization of the muscle cells, while the hyperpolarization elicited in the presence of calcium was sustained. The hyperpolarization is caused by enhancement of the potassium efflux assumed to be linked with mobilization of calcium form a cellular structure. Superfusion of the preparation with calcium-containing solution to replenish the calcium store in the presence of procainamide (10 min) before the .alpha.1 response evoked in the absence of calcium and procainamide did not affect the transient hyperpolarization. Quinidine, however, suppressed the .alpha.1 response when the same procedure was followed. Both the transient and the sustained hyperpolarization evoked in smooth muscle cells in the presence of procainamide (15 min) or quinidine in calcium-containing or in calcium-free solution, respectively, were inhibited. The .alpha.1 response was reflected by a depolarization of the muscle cells after the potassium channels had been blocked with apamin (3 .times. 10-7 M, 20 min). The transient depolarization observed after .alpha.1-receptor stimulation under calcium-free conditions was also suppressed by procainamide and quinidine. These results can be explained by assuming that calcium mobilization, activated after stimulation of the .alpha.1-receptors, is inhibited by procainamide and quinidine. A possible additional effect of quinidine on replenishment of the calcium store from the extracellular space is not excluded.

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Accession: 006595979

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PMID: 2440706

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