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Role of muscular eNOS in skeletal arteries: endothelium-independent hypoxic vasoconstriction of the femoral artery is impaired in eNOS-deficient mice

Title
Role of muscular eNOS in skeletal arteries: endothelium-independent hypoxic vasoconstriction of the femoral artery is impaired in eNOS-deficient mice
Authors
Kim, Hae JinYoo, Hae YoungLin, Hai YueOh, Goo TaegZhang, Yin HuaKim, Sung Joon
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2016
Journal Title
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
ISSN
0363-6143JCR Link1522-1563JCR Link
Citation
vol. 311, no. 3, pp. C508 - C517
Keywords
endothelial nitric oxide synthasesmooth muscleskeletal arteryhypoxic vasoconstriction
Publisher
AMER PHYSIOLOGICAL SOC
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
We previously reported that hypoxia augments alpha-adrenergic contraction (hypoxic vasoconstriction, HVC) of skeletal arteries in rats. The underlying mechanism may involve hypoxic inhibition of endothelial nitric oxide synthase (eNOS) expressed in skeletal arterial myocytes (16). To further explore the novel role of muscular eNOS in the skeletal artery, we compared HVC in femoral arteries (FAs) from eNOS knockout (KO) mice with that from wild-type (WT) and heterozygous (HZ) mice. Immunohistochemical assays revealed that, in addition to endothelia, eNOS is also expressed in the medial layer of FAs, albeit at a much lower level. However, the medial eNOS signal was not evident in HZ FAs, despite strong expression in the endothelium; similar observations were made in WT carotid arteries (CAs). The amplitude of contraction induced by 1 mu M phenylephrine (PhE) was greater in HZ than in WT FAs. Hypoxia (3% PO2) significantly augmented PhE-induced contraction in WT FAs but not in HZ or KO FAs. No HVC was observed in PhE-pretreated WT CAs. The NOS inhibitor nitro-L-arginine methyl ester (0.1 mM) also augmented PhE contraction in endothelium-denuded WT FAs but not in WT CAs. Inhibitors specific to neuronal NOS and inducible NOS did not augment PhE-induced contraction of WT FAs. NADPH oxidase 4 (NOX4) inhibitor (GKT137831, 5 mu M), but not NOX2 inhibitor (apocynin, 100 mu M), suppressed HVC. Consistent with the role of reactive oxygen species (ROS), HVC was also inhibited by pretreatment with tiron or polyethylene glycol-catalase. Taken together, these data suggest that the eNOS expressed in smooth muscle cells in FAs attenuates alpha-adrenergic vasoconstriction; this suppression is alleviated under hypoxia, which potentiates vasoconstriction in a NOX4/ROS-dependent mechanism.
DOI
10.1152/ajpcell.00061.2016
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자연과학대학 > 생명과학전공 > Journal papers
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