Single isolated cells were obtained from the taenia of the guinea-pig's caecum by enzymic digestion and held under voltage clamp. The effects of various catecholamines, sympathomimetics and related compounds were tested for their ability to potentiate the voltage-dependent calcium current (ICa) evoked in these cells by a depolarizing step. 2. ICa was potentiated by up to 60% by isoprenaline, adrenaline, and noradrenaline which were equipotent. The EC50 for isoprenaline was about 40 nM. 3. The racemic mixtures of the optical isomers of isoprenaline, adrenaline, and noradrenaline, and (+)-isoprenaline, were equipotent with the (-)-isomers of these drugs. Dopamine, L-dopa, and catechol were equipotent with these catecholamines. 4. Removal or substitution of one or more of the hydroxy groups of the catechol moiety, as in phenylephrine, salbutamol, procaterol, methoxamine, terbutaline, BRL 37344, ICI 215001 or tyramine substantially reduced efficacy and/or potency. 5. The adrenoceptor blockers propranolol, phentolamine, dihydroergotamine, atenolol, CGP 20712A and ICI 118551, or the dopamine receptor blockers, haloperidol or flupenthixol, did not block the potentiating action of catechol or the catecholamines. 6. The receptor activated by catecholamines to increase ICa we suggest should be called a C-receptor in view of its sensitivity to catechol. It may arise by enzymic modification of a conventional adrenoceptor but its transduction also involves a novel mechanism which might indicate that it is present in the muscle cells before enzyme treatment.
