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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 2
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pubmed:dateCreated |
1996-1-16
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pubmed:abstractText |
The neurotransmitter substance P acts also as a potent vasodilator. Its participation in the pathogenesis of deoxycorticosterone acetate (DOCA)-salt hypertension was evaluated by an acute infusion of a newly synthesized, potent, specific nonpeptide antagonist of substance P at the NK-1 receptor, the agent CP 96,345. In conscious unrestrained rats, CP 96,345 induced significant and sustained increases in mean arterial pressure of DOCA-salt rats but only small, transient, and nonsignificant rises in blood pressure of sham-treated control rats. The rise in blood pressure was not accompanied by changes in heart rate. Maximal blood pressure increase in DOCA-salt rats was 31.7 +/- 14.8 mm Hg. In a second series of experiments, the hemodynamic effects of this antagonist were evaluated under anesthesia in both DOCA-salt and sham-treated control rats by the thermodilution method. During CP 96,345 infusion, sustained increases in cardiac index and stroke volume and decreases in total peripheral resistance were observed in both DOCA-salt and control rats. In DOCA-salt rats, cardiac index rose by 79.4%, while total peripheral resistance fell by 27.9% of the baseline values. In control rats, the changes were smaller (+27.2% and -22.5%, respectively). Stroke volume changed in parallel to cardiac output in both groups. The data suggest that acute blockade of NK-1 receptors increases blood pressure in DOCA-salt rats mainly by an increase in cardiac output. We conclude that endogenous substance P tends to counteract the DOCA-salt-induced elevation of blood pressure by modulating both cardiac output and peripheral resistance.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biphenyl Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/CP 96345,
http://linkedlifedata.com/resource/pubmed/chemical/Desoxycorticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Hypnotics and Sedatives,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurokinin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Substance P
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0194-911X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1186-9
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:7498993-Animals,
pubmed-meshheading:7498993-Biphenyl Compounds,
pubmed-meshheading:7498993-Blood Pressure,
pubmed-meshheading:7498993-Cardiac Output,
pubmed-meshheading:7498993-Cardiac Volume,
pubmed-meshheading:7498993-Desoxycorticosterone,
pubmed-meshheading:7498993-Heart Rate,
pubmed-meshheading:7498993-Hemodynamics,
pubmed-meshheading:7498993-Hypertension,
pubmed-meshheading:7498993-Hypnotics and Sedatives,
pubmed-meshheading:7498993-Male,
pubmed-meshheading:7498993-Rats,
pubmed-meshheading:7498993-Rats, Wistar,
pubmed-meshheading:7498993-Receptors, Neurokinin-1,
pubmed-meshheading:7498993-Sodium Chloride,
pubmed-meshheading:7498993-Substance P,
pubmed-meshheading:7498993-Vascular Resistance
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pubmed:year |
1995
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pubmed:articleTitle |
Cardiovascular effects of a specific nonpeptide antagonist of substance P (NK-1) receptor in DOCA-salt hypertension.
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pubmed:affiliation |
Nephrology Division, Escola Paulista de Medicina-Federal University of São Paulo, Brazil.
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pubmed:publicationType |
Journal Article,
Comparative Study
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