BACKGROUND: The aim of this study was to evaluate the characteristic features of the mechanical responses and membrane potential changes induced by remifentanil in human umbilical arteries (HUAs). The ionic mechanisms underlying the electrophysiological responses were pharmacologically assessed using two K(+) channel blockers. METHODS: Thirty-eight HUAs were obtained. Contraction-relaxation, membrane potential changes and electrical responses of the HUAs were recorded. RESULTS: Remifentanil produced concentration-dependent relaxation in both endothelium-intact and endothelium-denuded HUA rings. Remifentanil produced a significantly greater relaxation response in intact than in denuded HUA rings. In endothelium-intact rings, pre-treatment with L-nitroarginine [N(w)-NITRO-(L)-ARGININE (L-NO-ARG)] or indomethacin decreased the degree of remifentanil-induced relaxation. Remifentanil (10(-9)-10(-6) mol/l) produced a transient concentration-dependent membrane hyperpolarization, which was not decreased by pre-treatment with L-NO-ARG or indomethacin. It also produced a small concentration-dependent hyperpolarization in the presence of charybdotoxin or tetraethylammonium. CONCLUSION: In both endothelium-intact and endothelium-denuded HUAs, remifentanil induces concentration-dependent vasorelaxation and simultaneously releases nitric oxide, prostaglandins and possibly an endothelium-derived hyperpolarizing factor. In addition, it produces hyperpolarization in a dose-dependent manner. Hyperpolarization induced by remifentanil involves the activation of Ca(2+)-dependent and Ca(2+)-independent potassium channels regulated by intracellular Ca(2+).
BACKGROUND: The aim of this study was to evaluate the characteristic features of the mechanical responses and membrane potential changes induced by remifentanil in human umbilical arteries (HUAs). The ionic mechanisms underlying the electrophysiological responses were pharmacologically assessed using two K(+) channel blockers. METHODS: Thirty-eight HUAs were obtained. Contraction-relaxation, membrane potential changes and electrical responses of the HUAs were recorded. RESULTS:Remifentanil produced concentration-dependent relaxation in both endothelium-intact and endothelium-denuded HUA rings. Remifentanil produced a significantly greater relaxation response in intact than in denuded HUA rings. In endothelium-intact rings, pre-treatment with L-nitroarginine [N(w)-NITRO-(L)-ARGININE (L-NO-ARG)] or indomethacin decreased the degree of remifentanil-induced relaxation. Remifentanil (10(-9)-10(-6) mol/l) produced a transient concentration-dependent membrane hyperpolarization, which was not decreased by pre-treatment with L-NO-ARG or indomethacin. It also produced a small concentration-dependent hyperpolarization in the presence of charybdotoxin or tetraethylammonium. CONCLUSION: In both endothelium-intact and endothelium-denuded HUAs, remifentanil induces concentration-dependent vasorelaxation and simultaneously releases nitric oxide, prostaglandins and possibly an endothelium-derived hyperpolarizing factor. In addition, it produces hyperpolarization in a dose-dependent manner. Hyperpolarization induced by remifentanil involves the activation of Ca(2+)-dependent and Ca(2+)-independent potassium channels regulated by intracellular Ca(2+).