Document Detail


Role of the multidomain protein spinophilin in blood pressure and cardiac function regulation.
MedLine Citation:
PMID:  18711009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-18
Journal Detail:
Title:  Hypertension     Volume:  52     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-18     Completed Date:  2008-10-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  702-7     Citation Subset:  IM    
Affiliation:
Max Delbrück Center for Molecular Medicine, Berlin, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / 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:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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