Effects of vanadate on vascular contractility and membrane potential in the rabbit aorta.
- Author:
Sang Man CHUNG
1
;
Duck Sun AHN
;
Hye Sun SEOK
;
Yong JEONG
;
Bok Soom KANG
Author Information
- Publication Type:Original Article ; In Vitro ; Research Support, Non-U.S. Gov't
- Keywords: Vanadate; vascular smooth muscle; EDHF; rabbit thoracic aorta; ATP-sensitive K+ channel
- MeSH: Animal; Aorta/drug effects/physiology; In Vitro; Membrane Potentials/drug effects; Potassium/pharmacology; Potassium Channels/physiology; Rabbits; Support, Non-U.S. Gov't; Tetraethylammonium Compounds/pharmacology; Vanadates/*pharmacology; Vasodilation/*drug effects
- From:Yonsei Medical Journal 1992;33(1):14-23
- CountryRepublic of Korea
- Language:English
- Abstract: Isolated rabbit aortic ring with intact endothelial cell preparations precontracted with NE (10(-7) M) were relaxed by vanadate in a dose dependent manner (from 0.2 to 2 mM). Application of vanadate and ACh during the tonic phase of high K+(100 mM)-induced contraction showed a slight relaxation in contrast to that in NE-induced contraction, but sodium nitroprusside (10 microM) more effectively relaxed the aortic ring preparations in high K+ contraction than that of vanadate. Vanadate-induced relaxation in NE-contracted aortic rings was reversed by application of BaCl2 (50 microM) or glibenclamide (10 microM). Furthermore, Vanadate hyperpolarized membrane potential of smooth muscle cells in endothelium-intact aortic strips and this effect was abolished by application of glibenclamide. The above results suggest that vanadate release EDHF (Endothelium-Derived Hyperpolarizing Factor), in addition to EDRF (Endothelium-Derived Relaxing Factor) from endothelial cell. This EDHF hyperpolarize the smooth muscle cell membrane potential via opening of the ATP-sensitive K+ channel and close a voltage dependent Ca++ channel. So it is suggested that the vanadate-induced relaxation of rabbit thoracic aortic rings may be due to the combined effects of EDRF and EDHF.
