Key result
EDRF inhibitors and NOARG block ethanol tolerance in rat aortic rings, implicating EDRF release.
Why the study?
Tolerance to ethanol-induced contraction of the aorta is dependent on functional endothelial cells and may be mediated by endothelium-derived relaxing factor (EDRF).
Tolerance to ethanol-induced contraction in rat aorta appears to be mediated by the release of endothelium-derived relaxing factor (EDRF/nitric oxide).
Authors
No takes yet. Share an insight, caveat, or question.
Rat aortic EDRF findings warrant no clinical changes in alcohol management; leaves open human vascular translation and requires prospective study.
Edward T. Knych (1992) studied Ethanol-induced contraction of the aorta. Inhibitors of EDRF action (gossypol, pyrogallol, hemoglobin) and nitric oxide synthesis (NOARG) vs. Control animals / control values was evaluated on Expression of ethanol tolerance (shift in ethanol dose-response curve). In vitro pretreatment of aortic rings from ethanol-treated rats with EDRF inhibitors or NOARG inhibited the expression of ethanol tolerance, supporting that tolerance is mediated by EDRF release.
Synapse has enriched one closely related paper. Consider it for comparative context: