| pubmed-article:10051139 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10051139 | lifeskim:mentions | umls-concept:C0005768 | lld:lifeskim |
| pubmed-article:10051139 | lifeskim:mentions | umls-concept:C0206745 | lld:lifeskim |
| pubmed-article:10051139 | lifeskim:mentions | umls-concept:C0005847 | lld:lifeskim |
| pubmed-article:10051139 | lifeskim:mentions | umls-concept:C0907532 | lld:lifeskim |
| pubmed-article:10051139 | lifeskim:mentions | umls-concept:C0035028 | lld:lifeskim |
| pubmed-article:10051139 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10051139 | pubmed:dateCreated | 1999-5-3 | lld:pubmed |
| pubmed-article:10051139 | pubmed:abstractText | 1. Isometric tension was recorded in isolated rings of aorta, carotid, coronary and mesenteric arteries taken from endothelial nitric oxide synthase knockout mice (eNOS(-/-) mice) and the corresponding wild-type strain (eNOS(+/+) mice). The membrane potential of smooth muscle cells was measured in coronary arteries with intracellular microelectrodes. 2. In the isolated aorta, carotid and coronary arteries from the eNOS(+/+) mice, acetylcholine induced an endothelium-dependent relaxation which was inhibited by N(omega)-L-nitro-arginine. In contrast, in the mesenteric arteries, the inhibition of the cholinergic relaxation required the combination of N(omega)-L-nitro-arginine and indomethacin. 3. The isolated aorta, carotid and coronary arteries from the eNOS(-/-) mice did not relax in response to acetylcholine. However, acetylcholine produced an indomethacin-sensitive relaxation in the mesenteric artery from eNOS(-/-) mice. 4. The resting membrane potential of smooth muscle cells from isolated coronary arteries was significantly less negative in the eNOS(-/-) mice (-64.8 +/- 1.8 mV, n = 20 and -58.4 +/- 1.9 mV, n = 17, for eNOS(+/+) and eNOS(-/-) mice, respectively). In both strains, acetylcholine, bradykinin and substance P did not induce endothelium-dependent hyperpolarizations whereas cromakalim consistently produced hyperpolarizations (- 7.9 +/- 1.1 mV, n = 8 and -13.8 +/- 2.6 mV, n = 4, for eNOS(+/+) and eNOS(-/-) mice, respectively). 5. These findings demonstrate that in the blood vessels studied: (1) in the eNOS(+/+) mice, the endothelium-dependent relaxations to acetylcholine involve either NO or the combination of NO plus a product of cyclo-oxygenase but not EDHF; (2) in the eNOS(-/-) mice, NO-dependent responses and EDHF-like responses were not observed. In the mesenteric arteries acetylcholine releases a cyclo-oxygenase derivative. | lld:pubmed |
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| pubmed-article:10051139 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10051139 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10051139 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10051139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10051139 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10051139 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:10051139 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:VanhoutteP... | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:DuhaultJJ | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:FishmanM CMC | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:HuangP LPL | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:FélétouMM | lld:pubmed |
| pubmed-article:10051139 | pubmed:author | pubmed-author:ChataigneauTT | lld:pubmed |
| pubmed-article:10051139 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10051139 | pubmed:volume | 126 | lld:pubmed |
| pubmed-article:10051139 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10051139 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10051139 | pubmed:pagination | 219-26 | lld:pubmed |
| pubmed-article:10051139 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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