Stimulation by proctolin of the ouabain-insensitive sodium efflux in single barnacle muscle fibers.

A study has been made of the action of the neuropeptide proctolin on the radiosodium efflux from single barnacle muscle fibers. Proctolin (10(-8) M) when applied externally causes stimulation of the Na efflux in unpoisoned and ouabain-poisoned fibers. The response is prompt in onset, reaches a peak in 15 min and decays slowly. The response of the ouabain-insensitive Na efflux to external proctolin is dose-dependent, the concentration threshold being less than 10(-10) M. The response to proctolin is dependent on external Ca2+ but not on Na+. (i) The response to proctolin is abolished by high external Mg2+, as well as by verapamil, Co2+, Cd2+ and WB-4101. (ii) The response is also abolished by preinjecting 0.5 M MgCl2 or 0.1 M EGTA. The calmodulin antagonists trifluoperazine and imipramine are without effect on the response to proctolin. (i) Adenylate cyclase agonists, e.g. forskolin, fail to augment the response to proctolin. (ii) Prior injection of the phosphodiesterase inhibitors 1-propyl-3-methyl-7-(5-hydroxyhexyl)-xanthine (PMX) or 1-isoamyl-3-isobutylxanthine (IAX) fails to augment the response to proctolin. (iii) Prior injection of protein kinase inhibitor is ineffective. The response to proctolin is significantly reduced in the presence of tyramine. Taken together, these results support the view that proctolin stimulates the ouabain-insensitive Na efflux by activating Ca2+ channels and that the cAMP-protein kinase system is not involved in this response.