Glibenclamide relaxes vascular smooth muscle constriction produced by prostaglandin F2 alpha.
The present study has demonstrated: (1) glibenclamide can reduce resting tension in canine cerebral arteries but has no effect on resting tension in the rat aorta; (2) glibenclamide can relax prostaglandin F2 alpha-induced contractions in the rat aorta, and in canine femoral, mesenteric, renal, coronary, basilar and middle cerebral arteries; (3) the relaxation produced by glibenclamide in rat aorta is comparable to that of glyceryl trinitrate and stronger than that of papaverine; (4) canine femoral arteries are less sensitive to glibenclamide than the other arteries; (5) in cerebral arteries glibenclamide was as effective as papaverine, but less effective than glyceryl trinitrate; (6) the actions of glibenclamide on cerebral arteries are not mediated by cGMP as they were not blocked by methylene blue, an inhibitor of guanylate cyclase; (7) the effects of glibenclamide are not endothelium-dependent. The mechanism by which glibenclamide produces relaxation is not clear; while the drug is known to block ATP-dependent potassium channels, in vascular smooth muscle this would cause contraction, not dilation. The action of glibenclamide may be at the level of the receptor or the signal transduction process.
Zhang
H
H
Department of Surgery, University of Alberta, Edmonton, Canada.
Stockbridge
N
N
Weir
B
B
Krueger
C
C
Cook
D
D
D000818:Animals; D001158:Arteries / Q000187:drug effects; D015237:Dinoprost / Q000037:antagonists & inhibitors*; D004285:Dogs; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D005905:Glyburide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects
D015237:Dinoprost; D005905:Glyburide