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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-12-30
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pubmed:abstractText |
The purpose of this study was to determine the response of pulmonary vascular smooth muscle to (1) cellular depolarization (response to KC1), (2) alpha 1-adrenergic receptor stimulation (response to phenylephrine, epinephrine, and norepinephrine), and (3) eicosinoid receptor stimulation (response to prostaglandin F 2 alpha, serotonin, and U46619). Isolated rat pulmonary artery rings were suspended on a fine wire tensiometer in individual organ chambers. After confirming endothelial integrity (response to acetylcholine), dose-response curves were constructed for each vasoactive agonist. The maximal developed tension as well as the dose required to produce 50% of maximal contraction (EC50) was determined for each agonist. The U46619, a stable thromboxane A2 mimetic, and prostaglandin F 2 alpha, (PGF 2 alpha) produced the greatest maximal developed tension in pulmonary vascular smooth muscle. This maximal contraction to U46619 and PGF 2 alpha, was the same as the maximal tension in response to cellular depolarization (KCI). The maximal tension developed to KCI and U46619 was significantly greater than to alpha 1-adrenergic receptor stimulation and serotonin, 5HT. The maximal tension developed to PGF 2 alpha was greater than the developed tension to 5HT. The dose response curves of alpha 1-adrenergic receptor stimulation and U46619 were shifted to the left compared to PGF 2 alpha and 5HT. This study demonstrates that U46619, and PGF 2 alpha produce the greatest maximal developed tension in pulmonary vascular smooth muscle. Furthermore, U46619 has the same potency as alpha 1-adrenergic receptor stimulation, which is significantly greater than 5HT and PGF 2 alpha. These data may be helpful in the delineation of the pathophysiology of pulmonary hypertension due to adult respiratory distress syndrome.
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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 |
Feb
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pubmed:issn |
0022-4804
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
61
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
170-4
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8769962-Adrenergic alpha-Agonists,
pubmed-meshheading:8769962-Animals,
pubmed-meshheading:8769962-Dose-Response Relationship, Drug,
pubmed-meshheading:8769962-Muscle, Smooth, Vascular,
pubmed-meshheading:8769962-Potassium Chloride,
pubmed-meshheading:8769962-Pulmonary Artery,
pubmed-meshheading:8769962-Rats,
pubmed-meshheading:8769962-Rats, Sprague-Dawley,
pubmed-meshheading:8769962-Receptors, Eicosanoid,
pubmed-meshheading:8769962-Vasoconstriction
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pubmed:year |
1996
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pubmed:articleTitle |
Pulmonary vascular smooth muscle contraction.
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pubmed:affiliation |
Department of Surgery, University of Colorado Health Sciences Center, Denver, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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