Abstract
Abstract
The isometrically arranged kitten heart papillary muscle was used to study the depressant actions of cadmium ion (Cd2+) on heart muscle function. Although the Cd2+-induced decreases in papillary muscle tension development were dose dependent, peak tension was restored to pretreatment control only after the termination of 1 μM, but not 10 or 100 μM Cd2+ exposure. The Schild plot suggested that Cd2+ and Ca2+ are competitive antagonists but two additional observations indicated that noncompetitive mechanisms are also involved: (a) the contour of the tension twitch from the Cd2+-depressed muscle could not be restored to pre-cadmium control by increasing extracellular Ca2+ concentration, and (b) the contraction pattern after a reduction in external Ca2+ concentration from 2.0 to 0.5 mM differed from that after exposure to 25 μM Cd2+, even though both treatments depressed peak tension development by 80%. When the coronary-perfused rabbit heart was employed, left ventricular Ca concentration was not affected by perfusion with 100 μM Cd2+ even though mechanical function was obliterated by this dose. In conclusion, the mechanisms of action of Cd2+ are complex and do not appear to involve the displacement of Ca from the cardiac cell.
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