Bradykinin causes endothelium-independent hyperpolarisation and neuromodulation by prostanoid synthesis in hamster mesenteric artery.

The mechanism of bradykinin-induced hyperpolarisation and purinergic neuromodulation was examined in the hamster superior mesenteric artery using intracellular microelectrode techniques. Bradykinin induced a concentration-dependent hyperpolarisation both in endothelium-intact and -denuded preparations. Indomethacin blocked this hyperpolarisation. Prostacyclin and iloprost also hyperpolarised the membrane of mesenteric artery, while prostaglandin E(2) did not evoke any membrane hyperpolarisation. The bradykinin-, prostacyclin- and iloprost-induced hyperpolarisation were inhibited by glibenclamide. Bradykinin also inhibited the amplitude of the purinergic excitatory junction potentials (e.j.p.s), both in endothelium-intact and -denuded preparations. Indomethacin blocked this inhibitory effect. Prostaglandin E(2) inhibited the e.j. p. in a concentration-dependent manner. Focally applied ATP-induced depolarisation was not modified by bradykinin or prostaglandin E(2.) These findings suggest that bradykinin via prostanoids production pre-synaptically, inhibit the amplitude of purinergic e.j.p., resulting inhibitory purinergic neuromodulation. In addition, bradykinin-released prostanoids elicits membrane hyperpolarisation of smooth muscle cells through opening of K(ATP) channels.