Yonsei Med J.  1992 Mar;33(1):14-23. 10.3349/ymj.1992.33.1.14.

Effects of vanadate on vascular contractility and membrane potential in the rabbit aorta

• Chung SM
• Ahn DS
• Seok HS
• Jeong Y
• Kang BS

• KMID: 1117760
• DOI: http://doi.org/10.3349/ymj.1992.33.1.14

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.

Keyword

Vanadate; vascular smooth muscle; EDHF; rabbit thoracic aorta; ATP-sensitive K+ channel

MeSH Terms

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