Effects of vasopressin on smooth muscle cells of guinea-pig mesenteric vessels.
1 The effects of vasopressin on the membrane and contractile properties of smooth muscle cells of guinea-pig mesenteric arteries, and mesenteric and portal veins were investigated in various ionic environments by means of a micro-electrode technique and an isometric tension recording method. The results were compared with those obtained with oxytocin and noradrenaline (NA).2 In the mesenteric jejunal artery, the mean membrane potential was -56.6 +/- 2.3 mV, s.d, and the membrane was electrically quiescent. Application of outward current pulses generated small graded responses, and the current voltage relationship was linear with application of an inward current pulse.3 Vasopressin and NA depolarized the membrane and increased the membrane resistance. Vasopressin was a 1000 times more potent than oxytocin in depolarizing the membrane. In high concentrations, vasopressin (1 x 10(-3) or 1 x 10(-2) iu/ml) or NA (5.9 x 10(-5) M) generated slow oscillatory membrane potential changes (slow waves) and spikes during the depolarization. The excitatory actions of vasopressin and NA were not suppressed by tetrodotoxin (3.1 x 10(-7) M) or ouabain (1.3 x 10(-6) M) and the actions of vasopressin were not suppressed by adrenoceptor blocking agents (3.9 x 10(-7) M phentolamine or 3.6 x 10(-7) M propranolol).4 The depolarization induced by vasopressin or NA is mainly due to a decrease in the K-permeability of the membrane. However, the contribution of other ionic species to the depolarization induced by vasopressin or NA differed, e.g. in low concentrations of [Na](o), the NA-induced depolarization was suppressed to a greater extent than that due to vasopressin. In low concentrations of [Ca](o), the vasopressin-induced depolarization was suppressed to a greater extent than with NA.5 In low concentrations of [Ca](o) and in the presence of vasopressin or NA, spike generation was inhibited but slow waves were not. In low concentrations of [Na](o), the vasopressin-induced slow waves and spikes were for the great part preserved, but with a high concentration of [Ca](o), vasopressing-induced slow waves were suppressed.6 Both vasopressin and NA produced contractions in the jejunal mesenteric artery. However, the maximum contraction in response to vasopressin was larger than that to NA, although both induced similar membrane depolarization. In a low concentration of [Na](o), vasopressin but not NA produced a contraction.7 In the cranial mesenteric artery, NA (5.9 x 10(-5) M) depolarized the membrane and produced a contraction, while vasopressin (1 x 10(-1) iu/ml) and oxytocin (1 x 10(-1) iu/ml) neither depolarized the member nor produced a contraction. In the mesenteric vein, NA (5.9 x 10(-5) M) slightly depolarized the membrane and produced a small contraction. On the other hand, in the portal vein, NA (5.9 x 10(-7) M) produced a marked depolarization and a contraction. Vasopressin (1 x 10(-1) iu/ml) and oxytocin (1 x 10(-1) iu/ml) produced neither excitatory nor inhibitory actions in these veins.8 It is concluded that vasopressin acts on only small muscular arteries, while NA acts on all mesenteric vessels, particularly the portal vein. Therefore, the hepatic portal vascular resistance may be increased by NA and reduced by vasopressin.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D007583:Jejunum / Q000098:blood supply; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008638:Mesenteric Arteries / Q000187:drug effects*; D008642:Mesenteric Veins / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D010121:Oxytocin / Q000494:pharmacology; D011169:Portal Vein / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology*
D014667:Vasopressins; D010121:Oxytocin; D012964:Sodium; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine