| pubmed-article:12874096 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12874096 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:12874096 | lifeskim:mentions | umls-concept:C0020538 | lld:lifeskim |
| pubmed-article:12874096 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:12874096 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:12874096 | pubmed:dateCreated | 2003-10-3 | lld:pubmed |
| pubmed-article:12874096 | pubmed:abstractText | Recent reports have indicated that endothelin-induced vasoconstriction in isolated aortic vascular rings may be mediated by the production of superoxide anion. The purpose of this study was to determine the role of superoxide anion in mediating the chronic renal and hypertensive actions of endothelin. Endothelin-1 (5 pmol/kg per minute) was chronically infused into the jugular vein by use of mini-osmotic pump for 9 days in male Sprague-Dawley rats and in rats treated with the superoxide anion scavenger tempol (30 mg/kg per day). Mean arterial pressure in the endothelin-1-treated rats was 141+/-3 mm Hg, compared with 125+/-2 mm Hg in control rats. Endothelin-1 increased renal vascular resistance (15.3+/-2.5 versus 10+/-1.3 mm Hg/mL per minute) and decreased renal plasma flow (6.5+/-0.9 versus 8.7+/-0.7 mL/min) in control rats. Endothelin-1 also significantly increased TBARS in the kidney and urinary 8-isoprostaglandin F2alpha excretion. The increase in arterial pressure in response to endothelin-1 was completely abolished by tempol (127+/-4 versus 127+/-4 mm Hg). Tempol also markedly attenuated the renal plasma flow and renal vascular resistance response to endothelin-1. Tempol also significantly decreased the level of 8-isoprostaglandin F2alpha in the endothelin-1-treated rats. Tempol had no effect on arterial pressure or renal hemodynamics in control rats. These data indicate that formation of reactive oxygen species may play an important role in mediating hypertension induced by chronic elevations in endothelin. | lld:pubmed |
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| pubmed-article:12874096 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12874096 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12874096 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12874096 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12874096 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:AlexanderBarb... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:GrangerJoey... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:LlinasMaria... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:AbramSean RSR | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:ReckelhoffJan... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:SedeekMona... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:DrummondHeath... | lld:pubmed |
| pubmed-article:12874096 | pubmed:author | pubmed-author:FortepianiLou... | lld:pubmed |
| pubmed-article:12874096 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12874096 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:12874096 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12874096 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12874096 | pubmed:pagination | 806-10 | lld:pubmed |
| pubmed-article:12874096 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:12874096 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12874096 | pubmed:articleTitle | Role of reactive oxygen species in endothelin-induced hypertension. | lld:pubmed |
| pubmed-article:12874096 | pubmed:affiliation | Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss 39216-4505, USA. | lld:pubmed |
| pubmed-article:12874096 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12874096 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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