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  • Title: Differential blockade of potassium and carbachol contractures of toad isolated rectus abdominis muscle by calcium entry blockers, ketamine and hydrallazine.
    Author: Savage AO, Olokodana NA.
    Journal: Arch Int Pharmacodyn Ther; 1988; 291():175-84. PubMed ID: 3365061.
    Abstract:
    Contractures of the rectus abdominis muscle of Buffo regularis evoked by carbachol were inhibited in concentration-dependent fashion by verapamil, nifedipine, hydrallazine and ketamine, whereas KCI-induced contractures were relatively resistant to blockade by these compounds. The order of potency in blocking carbachol-induced responses was: verapamil greater than nifedipine greater than hydrallazine greater than ketamine, verapamil being over 10 times more potent than nifedipine. In high K+-depolarized muscles, carbachol elicited contractural responses which were inhibited by verapamil, nifedipine, hydrallazine and ketamine; these compounds exhibited similar blocking potencies against carbachol responses in high K+-depolarized muscles as in the polarized muscles. In Ca2+-free EGTA-Ringer's solution, both KCl and carbachol contractures were abolished, but were restored on readmission of Ca2+. d-Tubocurarine competitively antagonized carbachol, but not KCl contractures. It is suggested that (i) extracellular Ca2+-influx occurs during contractures of the toad rectus abdominis muscle induced by carbachol and KCl; (ii) there probably exists more than one pathway for Ca2+-entry into this muscle--one pathway is stimulated by high K+-depolarization, and another which is linked to the activation of nicotinic cholinoceptors. Verapamil, nifedipine, hydrallazine and ketamine appear to preferentially inhibit Ca2+-influx stimulated via a pathway linked to nicotinic cholinoceptors.
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