Source:http://linkedlifedata.com/resource/pubmed/id/15563533
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0014406,
umls-concept:C0038435,
umls-concept:C0079284,
umls-concept:C0205178,
umls-concept:C0205227,
umls-concept:C0597357,
umls-concept:C0599946,
umls-concept:C0871261,
umls-concept:C1414262,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1720127,
umls-concept:C2348358,
umls-concept:C2911692
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pubmed:issue |
4
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pubmed:dateCreated |
2005-3-17
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pubmed:abstractText |
Clinical studies have documented an abrupt rise in plasma endothelin-1 (ET-1) coincident with an increase in mean arterial pressure (MAP) during the response to acute stress. We therefore examined the ET(A) and ET(B) receptor-dependent effects of ET-1 on the pressor response to acute environmental stress in ET-1-dependent hypertension. Stress was induced by administration of air jet pulses (3 min) in ET(B) receptor-deficient (ET(B) sl/sl) rats fed normal salt (NS; 0.8% NaCl), high salt (HS; 8% NaCl), and HS plus the ET(A) receptor antagonist ABT-627 (5 mg.kg(-1).day(-1)) on successive weeks. MAP was chronically monitored by telemetry. Total pressor response (area under the curve) was significantly reduced in ET(B) sl/sl rats maintained on a HS vs. NS diet [-6.8 mmHg (SD 18.7) vs. 29.3 mmHg (SD 8.1) x 3 min, P < 0.05]. Conversely, the total pressor response was augmented in both wild-type [34.2 mmHg (SD 29.2) x 3 min, P < 0.05 vs. NS] and ET(B) sl/sl rats [49.1 mmHg (SD 11.8) x 3 min, P < 0.05 vs. NS] by ABT-627. Blockade of ET(B) receptors in Sprague-Dawley rats caused an increase in basal MAP that was enhanced by HS and lowered by mixed ET(A)/ET(B) receptor antagonism; none of these treatments, however, had any effect on the pressor response. These data demonstrate that increasing endogenous ET-1 suppresses the pressor response to acute stress through ET(A) receptor activation in a genetic model of ET-1-dependent hypertension. These results are consistent with reports that ET-1 can attenuate sympathetically mediated responses.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
288
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1829-35
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15563533-Acute Disease,
pubmed-meshheading:15563533-Air Movements,
pubmed-meshheading:15563533-Animals,
pubmed-meshheading:15563533-Endothelin-1,
pubmed-meshheading:15563533-Hypertension,
pubmed-meshheading:15563533-Male,
pubmed-meshheading:15563533-Rats,
pubmed-meshheading:15563533-Rats, Inbred Dahl,
pubmed-meshheading:15563533-Rats, Mutant Strains,
pubmed-meshheading:15563533-Rats, Sprague-Dawley,
pubmed-meshheading:15563533-Receptor, Endothelin A,
pubmed-meshheading:15563533-Receptor, Endothelin B,
pubmed-meshheading:15563533-Sodium Chloride, Dietary,
pubmed-meshheading:15563533-Stress, Physiological,
pubmed-meshheading:15563533-Sympathetic Nervous System
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pubmed:year |
2005
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pubmed:articleTitle |
Endogenous endothelin attenuates the pressor response to acute environmental stress via the ETA receptor.
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pubmed:affiliation |
Vascular Biology Center and Department of Physiology, Medical College of Georgia, 1459 Laney Walker Blvd., Augusta, GA 30912-2500, USA. gdangelo@mail.mcg.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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