pubmed-article:1551193 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1551193 | lifeskim:mentions | umls-concept:C0034705 | lld:lifeskim |
pubmed-article:1551193 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
pubmed-article:1551193 | lifeskim:mentions | umls-concept:C0025465 | lld:lifeskim |
pubmed-article:1551193 | lifeskim:mentions | umls-concept:C0001041 | lld:lifeskim |
pubmed-article:1551193 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
pubmed-article:1551193 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:1551193 | pubmed:dateCreated | 1992-4-24 | lld:pubmed |
pubmed-article:1551193 | pubmed:abstractText | The endothelium-dependent vascular relaxation to acetylcholine (ACh) in spontaneously hypertensive rats (SHR) may be impaired because of an imbalance of endothelium-derived relaxing factor and contracting factor. However, the role of the endothelium-dependent hyperpolarization remains undetermined. We examined the ACh-induced hyperpolarization and its contribution to relaxation in arteries of SHR. Membrane potentials were recorded from the mesenteric artery trunk of 6-8-month-old male SHR and also Wistar-Kyoto (WKY) rats. Endothelium-dependent hyperpolarization to ACh was unaffected by NG-nitro-L-arginine, indomethacin, or glibenclamide; was reduced by tetraethylammonium or high K+ solution; and was enhanced by low K+ solution or methylene blue, thereby indicating that hyperpolarization is not mediated by nitric oxide (endothelium-derived relaxing factor) but is presumably mediated by a hyperpolarizing factor and is due to an opening of K+ channels that probably differ from the ATP-sensitive ones. Hyperpolarizations to ACh were markedly reduced in SHR compared with findings in WKY rats (maximum, 8 +/- 1 versus 17 +/- 1 mV). In addition, under conditions of depolarization with norepinephrine (10(-5) M), the ACh-induced hyperpolarization was even less and transient in SHR, while it was large and sustained in WKY rats (6 +/- 1 versus 29 +/- 2 mV). Endothelium-dependent relaxations to ACh in arterial rings precontracted with 10(-5) M norepinephrine were far less in SHR than in WKY rats, even in the presence of indomethacin. Furthermore, high K+ solution showed smaller inhibitory effects on the relaxations in SHR than in WKY rats. Endothelium-independent hyperpolarizations and relaxations to cromakalim, a K+ channel opener, were similar between SHR and WKY rats. It would thus appear that the endothelium-dependent hyperpolarization to ACh is reduced in SHR and this would, in part, account for the impaired relaxation to ACh in SHR mesenteric arteries. | lld:pubmed |
pubmed-article:1551193 | pubmed:language | eng | lld:pubmed |
pubmed-article:1551193 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1551193 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1551193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1551193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1551193 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1551193 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1551193 | pubmed:month | Apr | lld:pubmed |
pubmed-article:1551193 | pubmed:issn | 0009-7330 | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:FujishimaMM | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:KobayashiKK | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:TominagaMM | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:FujiiKK | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:TakataYY | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:KogaTT | lld:pubmed |
pubmed-article:1551193 | pubmed:author | pubmed-author:OhmoriSS | lld:pubmed |
pubmed-article:1551193 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1551193 | pubmed:volume | 70 | lld:pubmed |
pubmed-article:1551193 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1551193 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1551193 | pubmed:pagination | 660-9 | lld:pubmed |
pubmed-article:1551193 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:1551193 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1551193 | pubmed:articleTitle | Decreased endothelium-dependent hyperpolarization to acetylcholine in smooth muscle of the mesenteric artery of spontaneously hypertensive rats. | lld:pubmed |
pubmed-article:1551193 | pubmed:affiliation | Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan. | lld:pubmed |
pubmed-article:1551193 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1551193 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:1551193 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:1551193 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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