| Role of the multidomain protein spinophilin in blood pressure and cardiac function regulation. | |
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MedLine Citation:
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PMID: 18711009 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Andrey C da Costa-Goncalves; Jens Tank; Ralph Plehm; Andre Diedrich; Mihail Todiras; Maik Gollasch; Arnd Heuser; Maren Wellner; Michael Bader; Jens Jordan; Friedrich C Luft; Volkmar Gross |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-08-18 |
Journal Detail:
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Title: Hypertension Volume: 52 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-09-18 Completed Date: 2008-10-07 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 702-7 Citation Subset: IM |
Affiliation:
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Max Delbrück Center for Molecular Medicine, Berlin, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic alpha-Agonists
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pharmacology Adrenergic alpha-Antagonists / pharmacology Animals Autonomic Nervous System / drug effects, physiology Baroreflex / drug effects, physiology Blood Pressure / drug effects, physiology* Echocardiography, Stress Heart Rate / drug effects, physiology* Heart Ventricles / innervation, ultrasonography Male Mice Mice, Inbred C57BL Microfilament Proteins / metabolism* Nerve Tissue Proteins / metabolism* Phenylephrine / pharmacology Prazosin / pharmacology Signal Transduction Vasoconstriction / drug effects Ventricular Function |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic alpha-Agonists; 0/Adrenergic alpha-Antagonists; 0/Microfilament Proteins; 0/Nerve Tissue Proteins; 0/neurabin; 19216-56-9/Prazosin; 59-42-7/Phenylephrine |
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