The effects of two dihydropyridine calcium channel antagonists (nitrendipine and nifedipine) and two agonists (Bay K8644 and CGP-28392) were tested on high K(+)-induced contractures of frog's toe muscles. All four drugs depressed or blocked maximum contractures induced by 123 mM K+. Agonist effects, i.e., an increase in contracture amplitude, were found with smaller contractures produced by lower high K+ concentrations (i.e., 10, 20, and 25 mM). Bay K8644 produced its maximum agonist effect at 10(-7) M and only depressed contractures with 10(-6) M. CGP-28392 had its greatest agonist effect with 10(-9) M and had only antagonist effects with 10(-7) M or more. Nitrendipine had no agonist effects but nifedipine produced agonist effects with all concentrations tested (10(-9) to 10(-4) M). These results support previous results indicating that these contractures are initiated by extracellular Ca2+ ions entering via the voltage-sensitive, slow calcium channels in the t-tubules. The results obtained in the present study also are consistent with the known pharmacological effects of these drugs on calcium channels.