Effect of nitric oxide on membrane potential and contraction of rat aorta

Influence of nitric oxide (NO) on the membrane potential of rat aorta was assessed by blocking endothelial NO synthase with N omega-nitro-L-arginine (NOArg). Membrane potential was measured by two different methods: intracellular microelectrodes and [3H]tetraphenylphosphonium bromide ([3H]TPP+) uptake. Blocking of NO synthesis with NOArg (10(-4) M) depolarized the membrane by 4-6 mV. The NOArg-induced depolarization was suppressed by the NO donor SIN-1 (10(-5) M). Incubation with NOArg (10(-4) M) decreased the basal level of cGMP, and increased the basal 45Ca2+ influx as well as the sensitivity of contractile response to KCl. Results indicate that NO released by endothelial cells permanently hyperpolarizes the membrane of rat aorta smooth muscle cells and thereby may control the opening of voltage-dependent Ca2+ channels.