The effect of veratridine on sodium-sensitive radiocalcium uptake in frog sartorius muscle

Abstract

Veratridine increases the ability of sodium to displace calcium from muscle binding sites at physiological Ca 0 2+ concentrations of 1.0 mM. Lithium and hydrazine both of which can substitute for sodium with regard to the muscle action potential are much less effective in depressing calcium binding in the presence of veratridine. Lithium or hydrazine substitution for sodium prevents or delays the veratrine response. The uptake of 45Ca into the slow component of muscle as measured by 45Ca desaturation curves is enhanced by veratridine when the TTX treated sartorius muscle is exposed to 20 mM K +. Substitution of sodium by lithium or hydrazine does not interfere with the veratridine stimulated 45Ca uptake in the presence of high potassium. These findings indicate that veratridine affects calcium binding sites in the surface of the muscle fiber so as to increase the effectiveness of sodium in competing with calcium for these sites. Veratridine also appears to increase the transient calcium influx observed upon depolarization of the muscle fibers by high external potassium.