Source:http://linkedlifedata.com/resource/pubmed/id/11834493
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2002-2-8
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pubmed:abstractText |
The recent development of mice doubly deficient for monoamine oxidase A and B (MAO-A/B, respectively) has raised questions about the impact of these mutations on cardiovascular function, in so far as these animals demonstrate increased tissue levels of the vasoactive amines serotonin, norepinephrine, dopamine, and phenylethylamine. We recorded femoral arterial pressures and electrocardiograms in adult MAO-A/B-deficient mice during halothane-nitrous oxide anesthesia as well as 30 min postoperatively. During both anesthesia and recovery, systolic, diastolic, and mean arterial pressures were 10-15 mmHg lower in MAO-A/B-deficient mice compared with normal controls (P < 0.01). Mutants also showed a greater baroreceptor-mediated reduction in heart rate in response to hypertension after intravenous pulses of phenylephrine or angiotensin II. Tachycardia elicited in response to hypotension after nitroprusside was greater in mutants than in controls. Heart rate responsiveness to changes in arterial pressure was abolished after administration of glycopyrrolate, with no differences in this phenomenon noted between genotypes. These data suggest that prevention of hypertension may occur in chronic states of catecholaminergic/indoleaminergic excess by increased gain of the baroreflex.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Monoamine Oxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside,
http://linkedlifedata.com/resource/pubmed/chemical/Phenethylamines,
http://linkedlifedata.com/resource/pubmed/chemical/Propranolol,
http://linkedlifedata.com/resource/pubmed/chemical/phenethylamine
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
282
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H964-72
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11834493-Adrenergic beta-Antagonists,
pubmed-meshheading:11834493-Angiotensin II,
pubmed-meshheading:11834493-Animals,
pubmed-meshheading:11834493-Baroreflex,
pubmed-meshheading:11834493-Blood Pressure,
pubmed-meshheading:11834493-Electrocardiography,
pubmed-meshheading:11834493-Heart Rate,
pubmed-meshheading:11834493-Isoenzymes,
pubmed-meshheading:11834493-Mice,
pubmed-meshheading:11834493-Mice, Knockout,
pubmed-meshheading:11834493-Mice, Mutant Strains,
pubmed-meshheading:11834493-Monoamine Oxidase,
pubmed-meshheading:11834493-Nitroprusside,
pubmed-meshheading:11834493-Phenethylamines,
pubmed-meshheading:11834493-Pressoreceptors,
pubmed-meshheading:11834493-Propranolol,
pubmed-meshheading:11834493-Sequence Deletion
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pubmed:year |
2002
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pubmed:articleTitle |
Increased baroreceptor response in mice deficient in monoamine oxidase A and B.
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pubmed:affiliation |
Department of Psychiatry and the Behavioral Sciences, Keck School of Medicine, LAC-USC Hosp, University of Southern California Los Angeles 90024, USA. holschne@hsc.usc.edu.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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