Source:http://linkedlifedata.com/resource/pubmed/id/11208569
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2001-3-14
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| pubmed:abstractText |
Whereas previous studies have established that many mechanisms mediating pharmacomechanical coupling are subject to regulation, evidence of physiological regulation of the coupling efficiency between receptor activation and second-messenger production is scarce. The present studies address the hypothesis that acute hypoxia and maturation can influence the mass of second-messenger production for each activated agonist-bound receptor ("receptor gain"). For this assessment, receptor density and agonist affinity values were used to calculate 5-hydroxytryptamine (5-HT) concentrations that would produce standardized numbers of bound receptors (8.5 fmol/mg protein) in each experimental group and thus minimize effects of age or hypoxia on receptor density or agonist affinity. After 3 min of exposure to these 5-HT concentrations, normoxic magnitudes of contraction were similar (as %potassium maxima) in fetal (50 +/- 14%) and adult (40 +/- 9%) arteries, but hypoxia (PO(2) approximately 9--12 Torr for 30 min) depressed contractile tensions with a significantly different time course and magnitude in fetal (30 +/- 10%) and adult (17 +/- 11%) arteries (P < 0.05). Basal inositol 1,4,5-trisphosphate (IP(3)) values (in pmol/mg protein) were significantly greater in fetal (94 +/- 16) than in adult (44 +/- 6) arteries, and integrated areas above baseline for the IP(3) time courses (in nmol-s/mg protein) were significantly greater in fetal than in adult arteries both in normoxic (14.3 +/- 1.8 vs. 9.1 +/- 1.6) and hypoxic (15.0 +/- 2.1 vs. 8.6 +/- 1.2) conditions (P < 0.05). Hypoxia altered the IP(3) time courses both in the fetus and the adult but had no significant effect on IP(3 )mobilization or receptor gain. These data demonstrate that for the 5-HT(2a) receptor predominant in this preparation, receptor gain can be experimentally determined, is not influenced by acute hypoxia, but is greater in fetal than in adult ovine carotid arteries.
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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/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0363-6119
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
280
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
R410-7
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| pubmed:dateRevised |
2007-7-18
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| pubmed:meshHeading |
pubmed-meshheading:11208569-Animals,
pubmed-meshheading:11208569-Anoxia,
pubmed-meshheading:11208569-Calcium Channels,
pubmed-meshheading:11208569-Carotid Artery, Common,
pubmed-meshheading:11208569-Female,
pubmed-meshheading:11208569-Fetal Hypoxia,
pubmed-meshheading:11208569-Fetus,
pubmed-meshheading:11208569-Gestational Age,
pubmed-meshheading:11208569-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:11208569-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:11208569-Male,
pubmed-meshheading:11208569-Muscle, Smooth, Vascular,
pubmed-meshheading:11208569-Muscle Contraction,
pubmed-meshheading:11208569-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:11208569-Pregnancy,
pubmed-meshheading:11208569-Receptor Cross-Talk,
pubmed-meshheading:11208569-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:11208569-Second Messenger Systems,
pubmed-meshheading:11208569-Serotonin,
pubmed-meshheading:11208569-Sheep
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| pubmed:year |
2001
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| pubmed:articleTitle |
Effects of maturation and acute hypoxia on receptor-IP(3) coupling in ovine common carotid arteries.
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| pubmed:affiliation |
Center for Perinatal Biology, Department of Physiology, Loma Linda University School of Medicine, Loma Linda, California 92350, USA.
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| pubmed:publicationType |
Journal Article
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