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Increased activation of BKCa channels prevents endothelial dysfunction in coronary arteries from ouabain‐induced hypertensive rats
Author(s) -
Briones Ana M,
Cobeño Laura,
Padilha Alessandra S,
Cogolludo Angel,
Vassallo Dalton V,
PerezVizcaino Francisco,
Salaices Mercedes
Publication year - 2008
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.22.1_supplement.914.6
Subject(s) - iberiotoxin , ouabain , chemistry , acetylcholine , medicine , endocrinology , vasodilation , nitric oxide , coronary arteries , endothelium , artery , sodium , organic chemistry
Chronic ouabain administration induces hypertension. The aim of this study was to compare the endothelium‐dependent relaxation in coronary arteries (CA) isolated from ouabain‐treated versus non‐treated Wistar rats. In 5HT precontracted arteries, acetylcholine (Ach) induced similar relaxant responses in CA from both groups, and this relaxant effect was abolished by the nitric oxide synthase inhibitor L‐NAME. However, when arteries were contracted with high KCl or preincubated with the BKCa channel inhibitor iberiotoxin, but not with the Kv channel blocker 4‐aminopyridine, the relaxation elicited by Ach was more reduced in ouabain‐treated than control rats. Similar results were obtained with the NO donor DEA‐NO in endothelium‐denuded CA. In CA myocytes isolated from ouabain‐treated, but not from non‐treated rats, addition of DEA‐NO (1 μM) markedly increased the amplitude of the iberiotoxin‐sensitive current in the whole range of test potentials. This effect was prevented by the soluble guanylate cyclase inhibitor ODQ. Our results suggest that an increased activation of BKCa channels by NO prevents endothelial dysfunction in CA from ouabain‐treated rats. Supported by AGL2004‐06685/ALI, SAF2005‐03770, Fundacion Mutua Madrileña, SAF2006‐02376 and RECAVA RD06/0014/0011