Abstract

In isolated rabbit left atria Cd⁺⁺ (0.02-0.5 mM) caused a marked depression of the action potential and a slight decrease in time resting potential and the 10% duration. In more than half of the atria exposed to 0.5 mM Cd⁺⁺, action potentials were totally abolished with a slight reduction of the resting potential. Parameters of the transmembrarne potential recorded from control preparations were not affected by cysteine (1 mM). The inhibitory effect of Cd⁺⁺ was partly reversed by cysteine, excess Ca⁺⁺ and ethylene glycol bis(aminoethyl ether)-N,N,N',N'-tetraacetic acid. In atria in which action potentials were totally abolished by 0.5 mM Cd⁺⁺, these agents restored the action potentials. Cysteine was the most effective. The contractile force-rate curve of left atria was significantly depressed by Cd⁺⁺ (0.02 and 0.1 mM). The inhibitory effect of Cd⁺⁺ was reversed by cysteine in concentrations insufficient, to alter contractility in control media and also by excess Ca⁺⁺. It appears that the Cd⁺⁺-induced depression of action potentials and contractions is due to binding with sulfhydryl groups in membrarnes and contractile proteins as well as interference with availability and inward movements of Ca⁺⁺. It is concluded that membrane sulfhydryl groups may relate closely to the permeability of atrial cell membranes to Na⁺ and Ca⁺⁺ during excitation.