Differential blockade of potassium and carbachol contractures of toad isolated rectus abdominis muscle by calcium entry blockers, ketamine and hydrallazine
Savage, A.O.; Olokodana, N.A.
Archives Internationales de Pharmacodynamie et de Therapie 291: 175-184
1988
ISSN/ISBN: 0003-9780 PMID: 3365061 Document Number: 318751
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 > nifedipine > hydrallazine > 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 KC1 and carbachol contractures were abolished, but were restored on readmission of Ca2+. d-Tubocurarine competitively antagonized carbachol, but not KCl contactures. It is suggested that (i) extracellular Ca2+-influx occurs during contractures of the toad rectus abdominis muscle induced by carbachol and KC1; (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.