pubmed-article:11353669 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C0003009 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C0542331 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C1417869 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C1442858 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
pubmed-article:11353669 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:11353669 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:11353669 | pubmed:dateCreated | 2001-5-16 | lld:pubmed |
pubmed-article:11353669 | pubmed:abstractText | Recent studies have suggested that the central nervous system is responsible for activation of sympathetic nerve activity (SNA) and the renin-angiotensin system in heart failure (HF). The aim of this study was to determine whether activation of the renin-angiotensin system within the nucleus of the solitary tract (NTS) plays a role in enhanced SNA in HF. High-output HF was induced by an aortocaval (A-V) shunt with some modifications in the rat. These rats exhibited a left ventricular dilatation and hemodynamic signs of high-output HF. Urinary catecholamine excretion and maximal renal SNA (RSNA) were greater in the A-V shunted rats than in the control rats. Microinjection of an angiotensin II type 1-receptor antagonist, CV11974, into the NTS was performed. The arterial pressure and RSNA were reduced by CV11974 to a greater degree in the A-V shunted rats than in the control rats. The expression of angiotensin-converting enzyme mRNA in the medulla was greater in the A-V shunted rats than in the control rats. These results suggest that activation of the renin-angiotensin system within the NTS contributes to an enhanced SNA in this model. | lld:pubmed |
pubmed-article:11353669 | pubmed:language | eng | lld:pubmed |
pubmed-article:11353669 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11353669 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11353669 | pubmed:month | Jun | lld:pubmed |
pubmed-article:11353669 | pubmed:issn | 0363-6119 | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:ShigematsuHH | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:HirookaYY | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:TakeshitaAA | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:TagawaTT | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:EshimaKK | lld:pubmed |
pubmed-article:11353669 | pubmed:author | pubmed-author:ShiharaMM | lld:pubmed |
pubmed-article:11353669 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11353669 | pubmed:volume | 280 | lld:pubmed |
pubmed-article:11353669 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11353669 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11353669 | pubmed:pagination | R1665-73 | lld:pubmed |
pubmed-article:11353669 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:11353669 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11353669 | pubmed:articleTitle | Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt. | lld:pubmed |
pubmed-article:11353669 | pubmed:affiliation | Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. | lld:pubmed |
pubmed-article:11353669 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11353669 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11353669 | lld:pubmed |