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Resveratrol can enhance as well as relax contractions of the rat tail artery. Possible role of endothelial potassium channels
Author(s) -
Peuler Jacob D.,
Stom Sayra M.,
Phelps Laura E.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.940.2
Subject(s) - glibenclamide , resveratrol , tetraethylammonium , potassium channel , contraction (grammar) , chemistry , potassium , pharmacology , potassium channel blocker , medicine , vascular smooth muscle , artery , endocrinology , anesthesia , smooth muscle , organic chemistry , diabetes mellitus
Last year we reported that resveratrol can directly relax adrenergically‐precontracted rings prepared from the ventral tail artery of the rat (FASEB J. 29, supplement 1, 783.6, 2015). In addition, this effect was no different in proximal (conductance) vs. distal (resistance) portions of the same vessel. Our present aim was to determine if that relaxation could be blocked by agents known to block different subpopulations of potassium (K) channels in arterial smooth muscle. We found that it could not. However, we uncovered a novel unanticipated action which has not been reported by others. In over half of our arterial ring preparations (proximal and distal alike), resveratrol enhanced the magnitude of adrenergically‐induced precontractions beginning well before its more delayed and sustained relaxant effect became apparent. Although transient in duration, this enhancing action lasted nearly two hours at the lower more therapeutically‐relevant test concentrations that we employed. This action provides the first reasonable explanation for previously unexplained increases in arterial pressures observed during acute intravenous administration of resveratrol to animal models of severe ischemic tissue injury, in which marked hypotension is often present and in need of correction. Also unanticipated, this same resveratrol‐induced enhancement of adrenergic contraction was notably inhibited by some of the same K channel blockers (particularly tetraethylammonium and glibenclamide) that failed to influence its relaxant effect. As smooth muscle is not a likely site for such a paradoxical finding, we suspect resveratrol is acting on K‐selective mechano‐sensitive ion channels located in the endothelium where they are thought to participate in release of contracting factors. Support or Funding Information Midwestern University Master's Program