Differential blockade of potassium and carbachol contractures of toad isolated rectus abdominis muscle by calcium entry blockers, ketamine and hydrallazine.

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.