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Connexin, BK, IK, and SK expression and EDHF in mouse mesenteric vasculature
Author(s) -
Triggle Chris,
Ceroni Lisa,
Jiang Yanfen,
Wiehler William,
Ellis Anthie,
Ding Hong
Publication year - 2006
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.20.5.a1175-c
Subject(s) - endothelium derived hyperpolarizing factor , apamin , charybdotoxin , prostacyclin , mesenteric arteries , chemistry , bradykinin , potassium channel , iberiotoxin , enos , vasodilation , calcium activated potassium channel , endothelium , medicine , nitric oxide , endocrinology , nitric oxide synthase , artery , receptor
Endothelium‐dependent vasodilatation (EDV) in the microcirculation is achieved by a combination of endothelium‐derived nitric oxide (NO), prostacyclin (PGI2) and endothelium‐derived hyperpolarizing factor (EDHF) with, as a generalization, the contribution of EDHF increasing inversely proportional to vessel size. The EDHF contribution to EDV is inhibited by a combination of the small and intermediate conductance calcium‐activated potassium channel, KCa, (SK and IK respectively) inhibitors apamin and charybdotoxin (or the more specific IK inhibitor TRAM‐34). Furthermore, myo‐endothelial gap junctions, made up of connexins (Cx), are likely key contributors to EDHF‐mediated EDV. In small mesenteric arteries (SMA) from the eNOS knock out mouse EDHF is the sole contributor to EDV, whereas in C57BL/6 mice EDV is mediated by NO + EDHF. In the present study we investigated the relative contribution of NO and EDHF in 1st vs. 2nd vs. 3rd order SMA from C57BL/6 mice and the ‘real‐time’ mRNA expression levels of IK, SK and BK (large conductance) channels and Cx 37, 40, 43 and 45 from C57BL/6 vs. eNOS −/−. Although the contribution of EDHF was greater in 3rd order vs. 2nd and greater in 2nd vs. 1st order vessels from C57BL/6 mice no difference, relative to the housekeeping gene beta‐actin, was found in expression levels of mRNA for SK1, SK2, SK3, IK, BK channels or Cx 37, 40, 43, 45; similar data was obtained in SMA from eNOS−/− mice. These data indicate that, at least at the level of mRNA, KCa channel and Cx expression in the SMA is not linked to expression of eNOS or the relative contribution of EDHF to EDV.