Source:http://linkedlifedata.com/resource/pubmed/id/18711009
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2008-9-18
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pubmed:abstractText |
Spinophilin controls intensity/duration of G protein-coupled receptor signaling and thereby influences synaptic activity. We hypothesize that spinophilin affects blood pressure through central mechanisms. We measured blood pressure and heart rate in SPL-deficient (SPL(-/-)), heterozygous SPL-deficient (SPL(+/-)), and wild-type (SPL(+/+)) mice by telemetry combined with fast Fourier transformation. We also assessed peripheral vascular reactivity and performed echocardiography. SPL(-/-) had higher mean arterial pressure than SPL(+/-) and SPL(+/+) (121+/-2, 112+/-1, and 113+/-1 mm Hg). Heart rate was inversely related to spinophilin expression (SPL(-/-) 565+/-0.4, SPL(+/-) 541+/-5, SPL(+/+) 525+/-8 bpm). The blood pressure response to prazosin, trimethapane, and the heart rate response to metoprolol were stronger in SPL(-/-) than SPL(+/+) mice, whereas heart rate response to atropine was attenuated in SPL(-/-). Mesenteric artery vasoreactivity after angiotensin II, phenylephrine, and the thromboxane mimetic (U46619) as well as change in heart rate, stroke volume, and cardiac output after dobutamine were similar in SPL(-/-) and SPL(+/+). Baroreflex sensitivity was attenuated in SPL(-/-) compared with SPL(+/-) and SPL(+/+), which was confirmed by pharmacological testing. Heart rate variability parameters were attenuated in SPL(-/-) mice. We suggest that an increase in central sympathetic outflow participates in blood pressure and heart rate increases in SPL(-/-) mice. The elevated blood pressure in SPL(-/-) mice was associated with attenuated baroreflex sensitivity and decreased parasympathetic activity. Our study is the first to show a role for the spinophilin gene in blood pressure regulation.
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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/Adrenergic alpha-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Microfilament Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Prazosin,
http://linkedlifedata.com/resource/pubmed/chemical/neurabin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1524-4563
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pubmed:author |
pubmed-author:BaderMichaelM,
pubmed-author:DiedrichAndreA,
pubmed-author:GollaschMaikM,
pubmed-author:GrossVolkmarV,
pubmed-author:HeuserArndA,
pubmed-author:JordanJensJ,
pubmed-author:LuftFriedrich CFC,
pubmed-author:PlehmRalphR,
pubmed-author:TankJensJ,
pubmed-author:TodirasMihailM,
pubmed-author:WellnerMarenM,
pubmed-author:da Costa-GoncalvesAndrey CAC
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pubmed:issnType |
Electronic
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
702-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:18711009-Adrenergic alpha-Agonists,
pubmed-meshheading:18711009-Adrenergic alpha-Antagonists,
pubmed-meshheading:18711009-Animals,
pubmed-meshheading:18711009-Autonomic Nervous System,
pubmed-meshheading:18711009-Baroreflex,
pubmed-meshheading:18711009-Blood Pressure,
pubmed-meshheading:18711009-Echocardiography, Stress,
pubmed-meshheading:18711009-Heart Rate,
pubmed-meshheading:18711009-Heart Ventricles,
pubmed-meshheading:18711009-Male,
pubmed-meshheading:18711009-Mice,
pubmed-meshheading:18711009-Mice, Inbred C57BL,
pubmed-meshheading:18711009-Microfilament Proteins,
pubmed-meshheading:18711009-Nerve Tissue Proteins,
pubmed-meshheading:18711009-Phenylephrine,
pubmed-meshheading:18711009-Prazosin,
pubmed-meshheading:18711009-Signal Transduction,
pubmed-meshheading:18711009-Vasoconstriction,
pubmed-meshheading:18711009-Ventricular Function
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pubmed:year |
2008
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pubmed:articleTitle |
Role of the multidomain protein spinophilin in blood pressure and cardiac function regulation.
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pubmed:affiliation |
Max Delbrück Center for Molecular Medicine, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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