Abstract

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.