Abstract

Several experimental approaches were utilized to obtain information concerning the mechanism by which nicotine acts to alter Ca⁴⁵ movements and induce contracture in frog sartorius muscle. Nicotine elicited an increased Ca⁴⁵ efflux only when EDTA was present in a Ca-free Ringer's bathing solution. Substitution of nitrate anion for chloride resulted in a potentiation of nicotine contracture but no additional Ca⁴⁵ uptake as measured by Ca⁴⁵ spaces after a 120-min washout. Increasing the potassium concentration to 80 mM markedly increased nicotine-C¹⁴ efflux but did not significantly alter the nicotine-C¹⁴ tissue space occupied. Neither nitrate anion nor 80 mM K⁺ altered intracellular pH as measured by DM0-C¹⁴ spaces. Also, high concentrations of d-tubocurarine chloride (0.3 mg/ml) did not prevent a nicotine contracture and associated increases in Ca45 uptake. These observations provide further indication that nicotine acts at sites in the transverse tubule membrane to alter Ca⁴⁵ movements and induce contracture. Furthermore, these actions of nicotine may occur at calcium sites different from those at which corresponding effects are elicited by exposure to 80 mM potassium.