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.
Wang
X
X
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Chu
W
W
Lau
F
F
van Breemen
C
C
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001011:Aorta; D001920:Bradykinin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D004357:Drug Synergism; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016257:Fura-2; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D011817:Rabbits
D000109:Acetylcholine; D001920:Bradykinin; D002118:Calcium; D016257:Fura-2