Mechanisms of VIP-induced inhibition of the lymphatic vessel pump
Identifieur interne : 002F82 ( Pmc/Corpus ); précédent : 002F81; suivant : 002F83Mechanisms of VIP-induced inhibition of the lymphatic vessel pump
Auteurs : Pierre-Yves Von Der Weid ; Sonia Rehal ; Peter Dyrda ; Stewart Lee ; Ryan Mathias ; Mozibur Rahman ; Simon Roizes ; Mohammad S. ImtiazSource :
- The Journal of Physiology [ 0022-3751 ] ; 2012.
Abstract
Lymphatic vessels serve as a route by which interstitial fluid, protein and other macromolecules are returned to the blood circulation and immune cells and antigens gain access to lymph nodes. Lymph flow is an active process promoted by rhythmical contraction–relaxation events occurring in the collecting lymphatic vessels. This lymphatic pumping is an intrinsic property of the lymphatic muscles in the vessel wall and consequent to action potentials. Compromised lymphatic pumping may affect lymph and immune cell transport, an action which could be particularly detrimental during inflammation. Importantly, many inflammatory mediators alter lymphatic pumping. Vasoactive intestinal peptide (VIP) is a neuro- and immuno-modulator thought to be released by nerve terminals and immune cells in close proximity to lymphatic vessels. We demonstrated the presence of the peptide in lymphatic vessels and in the lymph and examined the effects of VIP on mesenteric collecting lymphatic vessels of the guinea pig using pharmacological bioassays, intracellular microelectrode electrophysiology, immunofluorescence and quantitative real-time PCR. We showed that VIP alters lymphatic pumping by decreasing the frequency of lymphatic contractions and hyperpolarizing the lymphatic muscle membrane potential in a concentration-dependent manner. Our data further suggest that these effects are mainly mediated by stimulation of the VIP receptor VPAC2 located on the lymphatic muscle and the downstream involvement of protein kinase A (PKA) and ATP-sensitive K+ (KATP) channels. Inhibition of lymphatic pumping by VIP may compromise lymph drainage, oedema resolution and immune cell trafficking to the draining lymph nodes.
Url:
DOI: 10.1113/jphysiol.2012.230599
PubMed: 22451438
PubMed Central: 3424724
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PMC:3424724Le document en format XML
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<author><name sortKey="Von Der Weid, Pierre Yves" sort="Von Der Weid, Pierre Yves" uniqKey="Von Der Weid P" first="Pierre-Yves" last="Von Der Weid">Pierre-Yves Von Der Weid</name>
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<author><name sortKey="Rehal, Sonia" sort="Rehal, Sonia" uniqKey="Rehal S" first="Sonia" last="Rehal">Sonia Rehal</name>
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<author><name sortKey="Dyrda, Peter" sort="Dyrda, Peter" uniqKey="Dyrda P" first="Peter" last="Dyrda">Peter Dyrda</name>
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<author><name sortKey="Lee, Stewart" sort="Lee, Stewart" uniqKey="Lee S" first="Stewart" last="Lee">Stewart Lee</name>
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<author><name sortKey="Mathias, Ryan" sort="Mathias, Ryan" uniqKey="Mathias R" first="Ryan" last="Mathias">Ryan Mathias</name>
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<author><name sortKey="Rahman, Mozibur" sort="Rahman, Mozibur" uniqKey="Rahman M" first="Mozibur" last="Rahman">Mozibur Rahman</name>
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<author><name sortKey="Roizes, Simon" sort="Roizes, Simon" uniqKey="Roizes S" first="Simon" last="Roizes">Simon Roizes</name>
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<author><name sortKey="Imtiaz, Mohammad S" sort="Imtiaz, Mohammad S" uniqKey="Imtiaz M" first="Mohammad S" last="Imtiaz">Mohammad S. Imtiaz</name>
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<author><name sortKey="Von Der Weid, Pierre Yves" sort="Von Der Weid, Pierre Yves" uniqKey="Von Der Weid P" first="Pierre-Yves" last="Von Der Weid">Pierre-Yves Von Der Weid</name>
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<author><name sortKey="Rehal, Sonia" sort="Rehal, Sonia" uniqKey="Rehal S" first="Sonia" last="Rehal">Sonia Rehal</name>
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<author><name sortKey="Dyrda, Peter" sort="Dyrda, Peter" uniqKey="Dyrda P" first="Peter" last="Dyrda">Peter Dyrda</name>
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<author><name sortKey="Lee, Stewart" sort="Lee, Stewart" uniqKey="Lee S" first="Stewart" last="Lee">Stewart Lee</name>
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<author><name sortKey="Mathias, Ryan" sort="Mathias, Ryan" uniqKey="Mathias R" first="Ryan" last="Mathias">Ryan Mathias</name>
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<author><name sortKey="Rahman, Mozibur" sort="Rahman, Mozibur" uniqKey="Rahman M" first="Mozibur" last="Rahman">Mozibur Rahman</name>
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<author><name sortKey="Roizes, Simon" sort="Roizes, Simon" uniqKey="Roizes S" first="Simon" last="Roizes">Simon Roizes</name>
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<author><name sortKey="Imtiaz, Mohammad S" sort="Imtiaz, Mohammad S" uniqKey="Imtiaz M" first="Mohammad S" last="Imtiaz">Mohammad S. Imtiaz</name>
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<series><title level="j">The Journal of Physiology</title>
<idno type="ISSN">0022-3751</idno>
<idno type="eISSN">1469-7793</idno>
<imprint><date when="2012">2012</date>
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<front><div type="abstract" xml:lang="en"><p>Lymphatic vessels serve as a route by which interstitial fluid, protein and other macromolecules are returned to the blood circulation and immune cells and antigens gain access to lymph nodes. Lymph flow is an active process promoted by rhythmical contraction–relaxation events occurring in the collecting lymphatic vessels. This lymphatic pumping is an intrinsic property of the lymphatic muscles in the vessel wall and consequent to action potentials. Compromised lymphatic pumping may affect lymph and immune cell transport, an action which could be particularly detrimental during inflammation. Importantly, many inflammatory mediators alter lymphatic pumping. Vasoactive intestinal peptide (VIP) is a neuro- and immuno-modulator thought to be released by nerve terminals and immune cells in close proximity to lymphatic vessels. We demonstrated the presence of the peptide in lymphatic vessels and in the lymph and examined the effects of VIP on mesenteric collecting lymphatic vessels of the guinea pig using pharmacological bioassays, intracellular microelectrode electrophysiology, immunofluorescence and quantitative real-time PCR. We showed that VIP alters lymphatic pumping by decreasing the frequency of lymphatic contractions and hyperpolarizing the lymphatic muscle membrane potential in a concentration-dependent manner. Our data further suggest that these effects are mainly mediated by stimulation of the VIP receptor VPAC2 located on the lymphatic muscle and the downstream involvement of protein kinase A (PKA) and ATP-sensitive K<sup>+</sup>
(K<sub>ATP</sub>
) channels. Inhibition of lymphatic pumping by VIP may compromise lymph drainage, oedema resolution and immune cell trafficking to the draining lymph nodes.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Physiol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Physiol. (Lond.)</journal-id>
<journal-id journal-id-type="publisher-id">tjp</journal-id>
<journal-title-group><journal-title>The Journal of Physiology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0022-3751</issn>
<issn pub-type="epub">1469-7793</issn>
<publisher><publisher-name>Blackwell Science Inc</publisher-name>
<publisher-loc>Oxford, UK</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22451438</article-id>
<article-id pub-id-type="pmc">3424724</article-id>
<article-id pub-id-type="doi">10.1113/jphysiol.2012.230599</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Cardiovascular</subject>
</subj-group>
</article-categories>
<title-group><article-title>Mechanisms of VIP-induced inhibition of the lymphatic vessel pump</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>von der Weid</surname>
<given-names>Pierre-Yves</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Rehal</surname>
<given-names>Sonia</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Dyrda</surname>
<given-names>Peter</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Lee</surname>
<given-names>Stewart</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Mathias</surname>
<given-names>Ryan</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Rahman</surname>
<given-names>Mozibur</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Roizes</surname>
<given-names>Simon</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Imtiaz</surname>
<given-names>Mohammad S</given-names>
</name>
</contrib>
<aff><institution>Inflammation Research Network and Smooth Muscle Research Group, Snyder Institute of Infection, Immunity and Inflammation, Department of Physiology & Pharmacology, Faculty of Medicine, University of Calgary</institution>
<addr-line>Calgary, Alberta, Canada</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1"><bold>Corresponding author</bold>
P.-Y. von der Weid: Department of Physiology & Pharmacology, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1. Email: <email>vonderwe@ucalgary.ca</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>01</day>
<month>6</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>25</day>
<month>3</month>
<year>2012</year>
</pub-date>
<volume>590</volume>
<issue>Pt 11</issue>
<fpage>2677</fpage>
<lpage>2691</lpage>
<history><date date-type="received"><day>14</day>
<month>2</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>21</day>
<month>3</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>© 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<abstract><p>Lymphatic vessels serve as a route by which interstitial fluid, protein and other macromolecules are returned to the blood circulation and immune cells and antigens gain access to lymph nodes. Lymph flow is an active process promoted by rhythmical contraction–relaxation events occurring in the collecting lymphatic vessels. This lymphatic pumping is an intrinsic property of the lymphatic muscles in the vessel wall and consequent to action potentials. Compromised lymphatic pumping may affect lymph and immune cell transport, an action which could be particularly detrimental during inflammation. Importantly, many inflammatory mediators alter lymphatic pumping. Vasoactive intestinal peptide (VIP) is a neuro- and immuno-modulator thought to be released by nerve terminals and immune cells in close proximity to lymphatic vessels. We demonstrated the presence of the peptide in lymphatic vessels and in the lymph and examined the effects of VIP on mesenteric collecting lymphatic vessels of the guinea pig using pharmacological bioassays, intracellular microelectrode electrophysiology, immunofluorescence and quantitative real-time PCR. We showed that VIP alters lymphatic pumping by decreasing the frequency of lymphatic contractions and hyperpolarizing the lymphatic muscle membrane potential in a concentration-dependent manner. Our data further suggest that these effects are mainly mediated by stimulation of the VIP receptor VPAC2 located on the lymphatic muscle and the downstream involvement of protein kinase A (PKA) and ATP-sensitive K<sup>+</sup>
(K<sub>ATP</sub>
) channels. Inhibition of lymphatic pumping by VIP may compromise lymph drainage, oedema resolution and immune cell trafficking to the draining lymph nodes.</p>
</abstract>
</article-meta>
</front>
</pmc>
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