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  1. Book ; Online ; Thesis: Funktionelle Bedeutung des TRPV4-Kationenkanals bei endothelvermittelten Vasodilatationsprozessen

    Hartmannsgruber, Veronika [Verfasser]

    2010  

    Author's details vorgelegt von Veronika Hartmannsgruber
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Article ; Online: Vitamin D and central hypersensitivity in patients with chronic pain.

    von Känel, Roland / Müller-Hartmannsgruber, Veronika / Kokinogenis, Georgios / Egloff, Niklaus

    Pain medicine (Malden, Mass.)

    2014  Volume 15, Issue 9, Page(s) 1609–1618

    Abstract: Background: Low vitamin D is implicated in various chronic pain conditions with, however, inconclusive findings. Vitamin D might play an important role in mechanisms being involved in central processing of evoked pain stimuli but less so for spontaneous ...

    Abstract Background: Low vitamin D is implicated in various chronic pain conditions with, however, inconclusive findings. Vitamin D might play an important role in mechanisms being involved in central processing of evoked pain stimuli but less so for spontaneous clinical pain.
    Objective: This study aims to examine the relation between low serum levels of 25-hydroxyvitamin D3 (25-OH D) and mechanical pain sensitivity.
    Design: We studied 174 patients (mean age 48 years, 53% women) with chronic pain. A standardized pain provocation test was applied, and pain intensity was rated on a numerical analogue scale (0-10). The widespread pain index and symptom severity score (including fatigue, waking unrefreshed, and cognitive symptoms) following the 2010 American College of Rheumatology preliminary diagnostic criteria for fibromyalgia were also assessed. Serum 25-OH D levels were measured with a chemiluminescent immunoassay.
    Results: Vitamin deficiency (25-OH D < 50 nmol/L) was present in 71% of chronic pain patients; another 21% had insufficient vitamin D (25-OH D < 75 nmol/L). After adjustment for demographic and clinical variables, there was a mean ± standard error of the mean increase in pain intensity of 0.61 ± 0.25 for each 25 nmol/L decrease in 25-OH D (P = 0.011). Lower 25-OH D levels were also related to greater symptom severity (r = -0.21, P = 0.008) but not to the widespread pain index (P = 0.83) and fibromyalgia (P = 0.51).
    Conclusions: The findings suggest a role of low vitamin D levels for heightened central sensitivity, particularly augmented pain processing upon mechanical stimulation in chronic pain patients. Vitamin D seems comparably less important for self-reports of spontaneous chronic pain.
    MeSH term(s) Adult ; Aged ; Analgesics/therapeutic use ; Anticonvulsants/therapeutic use ; Antidepressive Agents/therapeutic use ; Calcifediol/blood ; Chronic Pain/blood ; Chronic Pain/epidemiology ; Chronic Pain/physiopathology ; Comorbidity ; Depression/drug therapy ; Depression/epidemiology ; Female ; Fibromyalgia/epidemiology ; Humans ; Hyperalgesia/diagnosis ; Hyperalgesia/epidemiology ; Hyperalgesia/etiology ; Hyperalgesia/physiopathology ; Male ; Middle Aged ; Overweight/epidemiology ; Pain Clinics ; Pain Measurement ; Pain Perception/physiology ; Pain Threshold ; Somatoform Disorders/epidemiology ; Vitamin D/physiology ; Vitamin D Deficiency/epidemiology ; Vitamin D Deficiency/physiopathology
    Chemical Substances Analgesics ; Anticonvulsants ; Antidepressive Agents ; Vitamin D (1406-16-2) ; Calcifediol (P6YZ13C99Q)
    Language English
    Publishing date 2014-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 2015903-1
    ISSN 1526-4637 ; 1526-2375
    ISSN (online) 1526-4637
    ISSN 1526-2375
    DOI 10.1111/pme.12454
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Arterial response to shear stress critically depends on endothelial TRPV4 expression.

    Hartmannsgruber, Veronika / Heyken, Willm-Thomas / Kacik, Michael / Kaistha, Anuradha / Grgic, Ivica / Harteneck, Christian / Liedtke, Wolfgang / Hoyer, Joachim / Köhler, Ralf

    PloS one

    2007  Volume 2, Issue 9, Page(s) e827

    Abstract: Background: In blood vessels, the endothelium is a crucial signal transduction interface in control of vascular tone and blood pressure to ensure energy and oxygen supply according to the organs' needs. In response to vasoactive factors and to shear ... ...

    Abstract Background: In blood vessels, the endothelium is a crucial signal transduction interface in control of vascular tone and blood pressure to ensure energy and oxygen supply according to the organs' needs. In response to vasoactive factors and to shear stress elicited by blood flow, the endothelium secretes vasodilating or vasocontracting autacoids, which adjust the contractile state of the smooth muscle. In endothelial sensing of shear stress, the osmo- and mechanosensitive Ca(2+)-permeable TRPV4 channel has been proposed to be candidate mechanosensor. Using TRPV4(-/-) mice, we now investigated whether the absence of endothelial TRPV4 alters shear-stress-induced arterial vasodilation.
    Methodology/principal findings: In TRPV4(-/-) mice, loss of the TRPV4 protein was confirmed by Western blot, immunohistochemistry and by in situ-patch-clamp techniques in carotid artery endothelial cells (CAEC). Endothelium-dependent vasodilation was determined by pressure myography in carotid arteries (CA) from TRPV4(-/-) mice and wild-type littermates (WT). In WT CAEC, TRPV4 currents could be elicited by TRPV4 activators 4alpha-phorbol-12,13-didecanoate (4alphaPDD), arachidonic acid (AA), and by hypotonic cell swelling (HTS). In striking contrast, in TRPV4(-/-) mice, 4alphaPDD did not produce currents and currents elicited by AA and HTS were significantly reduced. 4alphaPDD caused a robust and endothelium-dependent vasodilation in WT mice, again conspicuously absent in TRPV4(-/-) mice. Shear stress-induced vasodilation could readily be evoked in WT, but was completely eliminated in TRPV4(-/-) mice. In addition, flow/reperfusion-induced vasodilation was significantly reduced in TRPV4(-/-) vs. WT mice. Vasodilation in response to acetylcholine, vasoconstriction in response to phenylephrine, and passive mechanical compliance did not differ between genotypes, greatly underscoring the specificity of the above trpv4-dependent phenotype for physiologically relevant shear stress.
    Conclusions/significance: Genetically encoded loss-of-function of trpv4 results in a loss of shear stress-induced vasodilation, a response pattern critically dependent on endothelial TRPV4 expression. Thus, Ca(2+)-influx through endothelial TRPV4 channels is a molecular mechanism contributing significantly to endothelial mechanotransduction.
    MeSH term(s) Amino Acid Sequence ; Animals ; Carotid Arteries/metabolism ; Carotid Arteries/physiology ; Compliance ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiology ; Female ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Patch-Clamp Techniques ; Stress, Mechanical ; TRPV Cation Channels/chemistry ; TRPV Cation Channels/genetics ; TRPV Cation Channels/physiology ; Vasodilation
    Chemical Substances TRPV Cation Channels ; Trpv4 protein, mouse
    Language English
    Publishing date 2007-09-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0000827
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Arterial response to shear stress critically depends on endothelial TRPV4 expression.

    Veronika Hartmannsgruber / Willm-Thomas Heyken / Michael Kacik / Anuradha Kaistha / Ivica Grgic / Christian Harteneck / Wolfgang Liedtke / Joachim Hoyer / Ralf Köhler

    PLoS ONE, Vol 2, Iss 9, p e

    2007  Volume 827

    Abstract: BACKGROUND: In blood vessels, the endothelium is a crucial signal transduction interface in control of vascular tone and blood pressure to ensure energy and oxygen supply according to the organs' needs. In response to vasoactive factors and to shear ... ...

    Abstract BACKGROUND: In blood vessels, the endothelium is a crucial signal transduction interface in control of vascular tone and blood pressure to ensure energy and oxygen supply according to the organs' needs. In response to vasoactive factors and to shear stress elicited by blood flow, the endothelium secretes vasodilating or vasocontracting autacoids, which adjust the contractile state of the smooth muscle. In endothelial sensing of shear stress, the osmo- and mechanosensitive Ca(2+)-permeable TRPV4 channel has been proposed to be candidate mechanosensor. Using TRPV4(-/-) mice, we now investigated whether the absence of endothelial TRPV4 alters shear-stress-induced arterial vasodilation. METHODOLOGY/PRINCIPAL FINDINGS: In TRPV4(-/-) mice, loss of the TRPV4 protein was confirmed by Western blot, immunohistochemistry and by in situ-patch-clamp techniques in carotid artery endothelial cells (CAEC). Endothelium-dependent vasodilation was determined by pressure myography in carotid arteries (CA) from TRPV4(-/-) mice and wild-type littermates (WT). In WT CAEC, TRPV4 currents could be elicited by TRPV4 activators 4alpha-phorbol-12,13-didecanoate (4alphaPDD), arachidonic acid (AA), and by hypotonic cell swelling (HTS). In striking contrast, in TRPV4(-/-) mice, 4alphaPDD did not produce currents and currents elicited by AA and HTS were significantly reduced. 4alphaPDD caused a robust and endothelium-dependent vasodilation in WT mice, again conspicuously absent in TRPV4(-/-) mice. Shear stress-induced vasodilation could readily be evoked in WT, but was completely eliminated in TRPV4(-/-) mice. In addition, flow/reperfusion-induced vasodilation was significantly reduced in TRPV4(-/-) vs. WT mice. Vasodilation in response to acetylcholine, vasoconstriction in response to phenylephrine, and passive mechanical compliance did not differ between genotypes, greatly underscoring the specificity of the above trpv4-dependent phenotype for physiologically relevant shear stress. CONCLUSIONS/SIGNIFICANCE: Genetically encoded ...
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2007-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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