The Role of Membrane Depolarization in Norepinephrine-Induced Contractions of the Rabbit Mesenteric Resistance Artery

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Suzuki, N. and van Breemen, C. The role of membrane depolarization in norepinephrine-induced contractions of the rabbit mesenteric resistance artey. Japanese Journal of Smooth Muscle Research, 1986, 22 (5): 423-436 Changes in membrane potential during norepinephrine-induced contractions in the rabbit mesenteric resistance artery (3rd or 4th branch) were investigated using microelectrodes. Norepinephrine at concentrations greater than 10^-6 M depolarized the membrane and induced contractions dose-dependently. Maximum effects were produced by 10^-4 M norepinephrine. Depolarization was maintained at almost steady level during 15 Min application of norepinephrine. During the same period, contractions continued with slight decay. Oscillatory contractions were observed at more than 3×10^-6 M norepinephrine, and occasionally persisted throughout the application of norepinephrine. Treatments with Ca²⁺-rich 1 mM EGTA solution, 10^-5 M diltiazem, 3×10^-6 M D600 and 1 mM La³⁺ did not significantly affect the amount of depolarization induced by 10^-4 M norepinephrine; however, contractions were greatly inhibited by these treatments. Replacement of Na⁺ by choline markedly reduced depolarization while contractions were not affected. In Ca²⁺-free Na⁺-free solution, no depolarization was induced, while contractions were still produced by norepinephrine, indicating that Cl- was not essential for membrane depolarization. These results suggest that contractions of the rabbit mesenteric resistance artery to norepinephrine are mainly due to the enhanced influx of extracellular Ca²⁺ which is not dependent on potential-sensitive mechanisms. Depolarization is thought to be due to the increase in the membrane permeability to Na⁺ and Cl- which is coincidentally produced by norepinephrine. The membrane potential oscillations were dependent on Ca entry but could not be shown to be the result of fluctuations in Ca current.