Ca⁺⁺-kompetitive elektro-mechanische Entkoppelung durch Ni⁺⁺- und Co⁺⁺-Ionen am Warmblütermyokard

Abstract

Addition of 2 mM NiCl₂/l or CoCl₂ to a normal Tyrode solution containing 1,8 mM Ca⁺⁺/l can completely abolish the contractility of isolated guinea pig's papillary muscles without reducing the duration of the electrical excitation process. This effect can be fully explained by the assumption of a competitive antagonism between Ca⁺⁺ and these other bivalent cations on the contractile machinery. Therefore, even in the presence of Ni⁺⁺ or Co⁺⁺, excitation-contraction coupling is completely restored by excess Ca⁺⁺ (2–4 mM/l) within a few minutes. In contrast to these highly specific functions of Ca⁺⁺ in initiating the contractile events, replacement of Ca⁺⁺ by Ni⁺⁺ or Co⁺⁺ on the excitable surface membrane of the myocardial fibres does not lead to clear symptoms of Ca⁺⁺ deficiency as, for instance, to an abbreviation of action potential. Here, Ni⁺⁺ or Co⁺⁺ can even substitute Ca⁺⁺ by maintaining the normal shape of action potential in a Ca⁺⁺-deficient medium.