Bradykinin potentiates acetylcholine induced responses in native endothelial cells from rabbit aorta.

Membrane potential and intracellular [Ca2+] were measured in freshly isolated rabbit aortic endothelial cells. Acetylcholine (10 microM) induced transient membrane hyperpolarization and increased [Ca2+]i. Bradykinin (4 microM) had no direct effect on membrane potential or [Ca2+]i on its own, but potentiated the subsequent ACh response. It changed the usual transient ACh response to a maintained hyperpolarization. The maintained hyperpolarization was blocked by NiCl2 and TEA, indicating an involvement of receptor-operated-Ca2+ channel and Ca2+ -dependent K+ -channel activity. This potentiating effect on bradykinin in isolated cells was confirmed in organ bath studies using isolated aortic rings.