A Revisitation on the Mechanism of Action of KCI-lnduced Vascular Smooth Muscle Contraction: A Key Role of Cation Binding to the Plasma Membrane
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Aortic rings of Sprague-Dawley rats developed reproducible contractions in Ca-free, nominally Mg-free (2 microM), Na-free, K solution, but not in Ca-free, nominally Mg-free, K-free, Na solution. Further reduction of the residual Mg by 0.5 mM EDTA in the above solutions potentiated this K-induced contraction and allowed the development of a relatively small contraction in Na-rich medium, respectively. The amplitude of EDTA-enhanced, K-induced contraction was almost the same as the amplitude of contraction induced in K-rich ([K] = 142 mM), Ca-containing (2.5 mM) solution. Such K-induced contraction was completely inhibited by 38 mM Na and by 3 mM of Mg (and Ni or Cd). Nifedipine (1 microM) also inhibited aortic smooth muscle contraction produced in K-EDTA, Ca-free solution. Modulators of Ca in sarcoplasmic reticulum (ryanodine, caffeine and norephinephrine), Ca-ionophore (A-23187) and protein kinase C inhibitor (Calphostin C) had no effect on EDTA-enhanced, K-induced contraction. It was suggested that K-induced contraction in rat aorta is not dependent on the increase in cytosolic Ca following membrane depolarization, is not a result of the release of Ca from intracellular stores, and is not due to change of Ca sensitivity upon the activation of protein kinase C. We propose that the competition of K for Mg and Na at external binding sites on the plasma membranes of the smooth muscle cells is primarily responsible for the development of vascular contraction.
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