| pubmed-article:12691956 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12691956 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:12691956 | lifeskim:mentions | umls-concept:C0034052 | lld:lifeskim |
| pubmed-article:12691956 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:12691956 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:12691956 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:12691956 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12691956 | pubmed:dateCreated | 2003-7-9 | lld:pubmed |
| pubmed-article:12691956 | pubmed:abstractText | Nitric oxide (NO) donors generally relax vascular preparations through cGMP-mediated mechanisms. Relaxation of endothelium-denuded bovine pulmonary arteries (BPA) and coronary arteries to the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) is almost eliminated by inhibition of soluble guanylate cyclase activation with 10 microM 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), whereas only a modest inhibition of relaxation is observed under hypoxia (PO2 = 8-10 Torr). This effect of hypoxia is independent of the contractile agent used and is also observed with NO gas. ODQ eliminated SNAP-induced increases in cGMP under hypoxia in BPA. cGMP-independent relaxation of BPA to SNAP was not attenuated by inhibition of K+ channels (10 mM tetraethylammonium), myosin light chain phosphatase (0.5 microM microcystin-LR), or adenylate cyclase (4 microM 2',5'-dideoxyadenosine). SNAP relaxed BPA contracted with serotonin under Ca2+-free conditions in the presence of hypoxia and ODQ, and contraction to Ca2+ readdition was also attenuated. The sarcoplasmic reticulum Ca2+-reuptake inhibitor cyclopiazonic acid (0.2 mM) attenuated SNAP-mediated relaxation of BPA in the presence of ODQ. Thus hypoxic conditions appear to promote a cGMP-independent relaxation of BPA to NO by enhancing sarcoplasmic reticulum Ca2+ reuptake. | lld:pubmed |
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| pubmed-article:12691956 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12691956 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12691956 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12691956 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:12691956 | pubmed:issn | 1040-0605 | lld:pubmed |
| pubmed-article:12691956 | pubmed:author | pubmed-author:GupteSachin... | lld:pubmed |
| pubmed-article:12691956 | pubmed:author | pubmed-author:WolinMichael... | lld:pubmed |
| pubmed-article:12691956 | pubmed:author | pubmed-author:MingoneChrist... | lld:pubmed |
| pubmed-article:12691956 | pubmed:author | pubmed-author:IesakiTakafum... | lld:pubmed |
| pubmed-article:12691956 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12691956 | pubmed:volume | 285 | lld:pubmed |
| pubmed-article:12691956 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12691956 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12691956 | pubmed:pagination | L296-304 | lld:pubmed |
| pubmed-article:12691956 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:12691956 | pubmed:meshHeading | pubmed-meshheading:12691956... | lld:pubmed |
| pubmed-article:12691956 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12691956 | pubmed:articleTitle | Hypoxia enhances a cGMP-independent nitric oxide relaxing mechanism in pulmonary arteries. | lld:pubmed |
| pubmed-article:12691956 | pubmed:affiliation | Department of Physiology, New York Medical College, Valhalla, NY 10595, USA. mike_wolin@nymc.edu | lld:pubmed |
| pubmed-article:12691956 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12691956 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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