Karashima T, Itoh T, Kuriyama H
J Pharmacol Exp Ther. 1982 May;221(2):472-80.
The effects of 2-nicotinamidoethyl nitrate (2-NN) on the smooth muscle cells of the guinea-pig mesenteric and portal veins were investigated by using an intracellular microelectrode technique and isometric tension recording method. In the mesenteric vein, 2-NN (greater than 1 x 10(-5) M) hyperpolarized the membrane in a manner dependent on the dose. The 2-NN-induced hyperpolarization was also dependent on the external K concentration, but was independent of the external Na and Cl concentrations. It was unaffected by removal of Ca from the external solution. Therefore, the hyperpolarization is thought to be due to an increase in the K conductance of the membrane. Excess [K]0 depolarized the membrane and produced contraction. Although 2-NN (1 x 10(-6) M) did not modify the depolarization induced by excess [K]0. It suppressed the contraction. Norepinephrine depolarized and acetylcholine hyperpolarized the membrane, whereas both agents produced small concentrations. 2-NN (1 x 10(-4) M) suppressed the membrane potential changes and contractions evoked by both agents. In the portal vein, 2-NN (1 x 10(-5) M) also hyperpolarized the membrane and abolished the spontaneous spike generation and contraction. 2-NN is more potent on the mesenteric and portal veins than on the mesenteric artery.
采用细胞内微电极技术和等长张力记录方法,研究了2-烟酰胺基乙基硝酸盐(2-NN)对豚鼠肠系膜静脉和门静脉平滑肌细胞的影响。在肠系膜静脉中,2-NN(大于1×10⁻⁵M)以剂量依赖性方式使细胞膜超极化。2-NN诱导的超极化也依赖于细胞外钾浓度,但与细胞外钠和氯浓度无关。去除细胞外溶液中的钙对其无影响。因此,这种超极化被认为是由于细胞膜钾电导增加所致。细胞外高钾使细胞膜去极化并产生收缩。虽然2-NN(1×10⁻⁶M)不改变细胞外高钾诱导的去极化,但它抑制了收缩。去甲肾上腺素使细胞膜去极化,乙酰胆碱使细胞膜超极化,而这两种物质都产生较小的浓度变化。2-NN(1×10⁻⁴M)抑制了这两种物质引起的膜电位变化和收缩。在门静脉中,2-NN(1×10⁻⁵M)也使细胞膜超极化,并消除了自发的锋电位发放和收缩。2-NN对肠系膜静脉和门静脉的作用比对肠系膜动脉的作用更强。