Abstract
In the guinea-pig mesenteric artery, reduction in [Na]o by30mM (substituted by choline or sucrose;137mM [Na] o in Krebs solution) generated contraction with no change in membrane potential.In NaClfree solution (15mM [Na] o), the amplitude of phasic contraction reached 0.8times the contraction evoked by118mM [K] o with only a slight depolarization. In NaCl-free solution, the amplitude of phasic contrlction evoked by noradrenaline (NA) 5×10-5M or caffeine5mM increased to roughly twice the amplitude of the contraction evoked in the control solution. In Ca-free solution, the K-, NaCl-free-orNa-free-induced contractions rapidly ceased, but NA-inducfd contraction ceased within5min and the caffeine-induced contraction persisted for more than15min.In a skinned fiber, increase of [Na] o from10to60mM suppressed the pCa-tension relationship in the ranges of10-7and 10-5M free Ca but not with a dose of 30mM [Na] o.NA (10-5M) had no effect on skinned fibers. Increase in Na concentration (60mM) had no effect on Ca accumulation in the store site or on Ca release by caffeine.Possible Na-related mechanisms on the development of mechanical response are discussed in relation to Ca onthe surface and in the internal membrane structure.The NaC1- free-induced contraction in smooth muscles of the guinea-pig mesenteric artery is postulated to be due to influx of Ca through the Na channel, rather than the Ca channel.
