LymphedemaV1, PubMed, Checkpoint, bibRecord, 001515

Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.

Identifieur interne : 001515 ( PubMed/Checkpoint ); précédent : 001514; suivant : 001516

Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.

Auteurs : Niklas Telinius [Oman] ; Sheyanth Mohanakumar [Danemark] ; Jens Majgaard [Danemark] ; Sukhan Kim [Danemark] ; Hans Pilegaard [Danemark] ; Einar Pahle [Danemark] ; J Rn Nielsen [Danemark] ; Marc De Leval [Royaume-Uni] ; Christian Aalkjaer [Danemark] ; Vibeke Hjortdal [Danemark] ; Donna Briggs Boedtkjer [Danemark]

Source :

The Journal of physiology [ 1469-7793 ] ; 2014.

RBID : pubmed:25172950

Descripteurs français

KwdFr :
- Adulte, Adulte d'âge moyen, Canaux calciques de type L (génétique), Canaux calciques de type L (métabolisme), Conduit thoracique (), Conduit thoracique (cytologie), Conduit thoracique (physiologie), Contraction musculaire (), Humains, Inhibiteurs des canaux calciques (pharmacologie), Lymphoedème (), Lymphoedème (anatomopathologie), Myocytes du muscle lisse (), Mâle, Nifédipine (pharmacologie), Potentiels de membrane, Régulation de l'expression des gènes (), Sujet âgé, Sujet âgé de 80 ans ou plus, Techniques de culture de tissus, Études croisées.
MESH :
- anatomopathologie : Lymphoedème.
- cytologie : Conduit thoracique.
- génétique : Canaux calciques de type L.
- métabolisme : Canaux calciques de type L.
- pharmacologie : Inhibiteurs des canaux calciques, Nifédipine.
- physiologie : Conduit thoracique.
- Adulte, Adulte d'âge moyen, Conduit thoracique, Contraction musculaire, Humains, Lymphoedème, Myocytes du muscle lisse, Mâle, Potentiels de membrane, Régulation de l'expression des gènes, Sujet âgé, Sujet âgé de 80 ans ou plus, Techniques de culture de tissus, Études croisées.

English descriptors

KwdEn :
- Adult, Aged, Aged, 80 and over, Calcium Channel Blockers (pharmacology), Calcium Channels, L-Type (genetics), Calcium Channels, L-Type (metabolism), Cross-Over Studies, Gene Expression Regulation (drug effects), Humans, Lymphedema (chemically induced), Lymphedema (pathology), Male, Membrane Potentials, Middle Aged, Muscle Contraction (drug effects), Myocytes, Smooth Muscle (drug effects), Nifedipine (pharmacology), Thoracic Duct (cytology), Thoracic Duct (drug effects), Thoracic Duct (physiology), Tissue Culture Techniques.
MESH :
- chemical , genetics : Calcium Channels, L-Type.
- chemical , metabolism : Calcium Channels, L-Type.
- chemical , pharmacology : Calcium Channel Blockers, Nifedipine.
- chemically induced : Lymphedema.
- cytology : Thoracic Duct.
- drug effects : Gene Expression Regulation, Muscle Contraction, Myocytes, Smooth Muscle, Thoracic Duct.
- pathology : Lymphedema.
- physiology : Thoracic Duct.
- Adult, Aged, Aged, 80 and over, Cross-Over Studies, Humans, Male, Membrane Potentials, Middle Aged, Tissue Culture Techniques.

Abstract

Calcium channel blockers (CCB) are widely prescribed anti-hypertensive agents. The commonest side-effect, peripheral oedema, is attributed to a larger arterial than venous dilatation causing increased fluid filtration. Whether CCB treatment is detrimental to human lymphatic vessel function and thereby exacerbates oedema formation is unknown. We observed that spontaneous lymphatic contractions in isolated human vessels (thoracic duct and mesenteric lymphatics) maintained under isometric conditions were inhibited by therapeutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrations of verapamil (micromolar) were necessary to inhibit activity. Nifedipine also inhibited spontaneous action potentials measured by sharp microelectrodes. Furthermore, noradrenaline did not elicit normal increases in lymphatic vessel tone when maximal constriction was reduced to 29.4 ± 4.9% of control in the presence of 20 nmol l(-1) nifedipine. Transcripts for the L-type calcium channel gene CACNA1C were consistently detected from human thoracic duct samples examined and the CaV1.2 protein was localized by immunoreactivity to lymphatic smooth muscle cells. While human lymphatics ex vivo were highly sensitive to nifedipine, this was not apparent in vivo when nifedipine was compared to placebo in a randomized, double-blinded clinical trial: conversely, lymphatic vessel contraction frequency was increased and refill time was faster despite all subjects achieving target nifedipine plasma concentrations. We conclude that human lymphatic vessels are highly sensitive to nifedipine in vitro but that care must be taken when extrapolating in vitro observations of lymphatic vessel function to the clinical situation, as similar changes in lymphatic function were not evident in our clinical trial comparing nifedipine treatment to placebo.

DOI: 10.1113/jphysiol.2014.276683
PubMed: 25172950

Affiliations:

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Le document en format XML

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<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Calcium Channel Blockers (pharmacology)</term>
<term>Calcium Channels, L-Type (genetics)</term>
<term>Calcium Channels, L-Type (metabolism)</term>
<term>Cross-Over Studies</term>
<term>Gene Expression Regulation (drug effects)</term>
<term>Humans</term>
<term>Lymphedema (chemically induced)</term>
<term>Lymphedema (pathology)</term>
<term>Male</term>
<term>Membrane Potentials</term>
<term>Middle Aged</term>
<term>Muscle Contraction (drug effects)</term>
<term>Myocytes, Smooth Muscle (drug effects)</term>
<term>Nifedipine (pharmacology)</term>
<term>Thoracic Duct (cytology)</term>
<term>Thoracic Duct (drug effects)</term>
<term>Thoracic Duct (physiology)</term>
<term>Tissue Culture Techniques</term>
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<term>Adulte d'âge moyen</term>
<term>Canaux calciques de type L (génétique)</term>
<term>Canaux calciques de type L (métabolisme)</term>
<term>Conduit thoracique ()</term>
<term>Conduit thoracique (cytologie)</term>
<term>Conduit thoracique (physiologie)</term>
<term>Contraction musculaire ()</term>
<term>Humains</term>
<term>Inhibiteurs des canaux calciques (pharmacologie)</term>
<term>Lymphoedème ()</term>
<term>Lymphoedème (anatomopathologie)</term>
<term>Myocytes du muscle lisse ()</term>
<term>Mâle</term>
<term>Nifédipine (pharmacologie)</term>
<term>Potentiels de membrane</term>
<term>Régulation de l'expression des gènes ()</term>
<term>Sujet âgé</term>
<term>Sujet âgé de 80 ans ou plus</term>
<term>Techniques de culture de tissus</term>
<term>Études croisées</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Calcium Channel Blockers</term>
<term>Nifedipine</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lymphoedème</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Lymphedema</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Conduit thoracique</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Thoracic Duct</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term>
<term>Muscle Contraction</term>
<term>Myocytes, Smooth Muscle</term>
<term>Thoracic Duct</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Canaux calciques de type L</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Canaux calciques de type L</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphedema</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inhibiteurs des canaux calciques</term>
<term>Nifédipine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Conduit thoracique</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Thoracic Duct</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Cross-Over Studies</term>
<term>Humans</term>
<term>Male</term>
<term>Membrane Potentials</term>
<term>Middle Aged</term>
<term>Tissue Culture Techniques</term>
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<term>Adulte d'âge moyen</term>
<term>Conduit thoracique</term>
<term>Contraction musculaire</term>
<term>Humains</term>
<term>Lymphoedème</term>
<term>Myocytes du muscle lisse</term>
<term>Mâle</term>
<term>Potentiels de membrane</term>
<term>Régulation de l'expression des gènes</term>
<term>Sujet âgé</term>
<term>Sujet âgé de 80 ans ou plus</term>
<term>Techniques de culture de tissus</term>
<term>Études croisées</term>
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<front><div type="abstract" xml:lang="en">Calcium channel blockers (CCB) are widely prescribed anti-hypertensive agents. The commonest side-effect, peripheral oedema, is attributed to a larger arterial than venous dilatation causing increased fluid filtration. Whether CCB treatment is detrimental to human lymphatic vessel function and thereby exacerbates oedema formation is unknown. We observed that spontaneous lymphatic contractions in isolated human vessels (thoracic duct and mesenteric lymphatics) maintained under isometric conditions were inhibited by therapeutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrations of verapamil (micromolar) were necessary to inhibit activity. Nifedipine also inhibited spontaneous action potentials measured by sharp microelectrodes. Furthermore, noradrenaline did not elicit normal increases in lymphatic vessel tone when maximal constriction was reduced to 29.4 ± 4.9% of control in the presence of 20 nmol l(-1) nifedipine. Transcripts for the L-type calcium channel gene CACNA1C were consistently detected from human thoracic duct samples examined and the CaV1.2 protein was localized by immunoreactivity to lymphatic smooth muscle cells. While human lymphatics ex vivo were highly sensitive to nifedipine, this was not apparent in vivo when nifedipine was compared to placebo in a randomized, double-blinded clinical trial: conversely, lymphatic vessel contraction frequency was increased and refill time was faster despite all subjects achieving target nifedipine plasma concentrations. We conclude that human lymphatic vessels are highly sensitive to nifedipine in vitro but that care must be taken when extrapolating in vitro observations of lymphatic vessel function to the clinical situation, as similar changes in lymphatic function were not evident in our clinical trial comparing nifedipine treatment to placebo.</div>
</front>
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<Month>02</Month>
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</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1469-7793</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>592</Volume>
<Issue>21</Issue>
<PubDate><Year>2014</Year>
<Month>Nov</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>The Journal of physiology</Title>
<ISOAbbreviation>J. Physiol. (Lond.)</ISOAbbreviation>
</Journal>
<ArticleTitle>Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.</ArticleTitle>
<Pagination><MedlinePgn>4697-714</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1113/jphysiol.2014.276683</ELocationID>
<Abstract><AbstractText>Calcium channel blockers (CCB) are widely prescribed anti-hypertensive agents. The commonest side-effect, peripheral oedema, is attributed to a larger arterial than venous dilatation causing increased fluid filtration. Whether CCB treatment is detrimental to human lymphatic vessel function and thereby exacerbates oedema formation is unknown. We observed that spontaneous lymphatic contractions in isolated human vessels (thoracic duct and mesenteric lymphatics) maintained under isometric conditions were inhibited by therapeutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrations of verapamil (micromolar) were necessary to inhibit activity. Nifedipine also inhibited spontaneous action potentials measured by sharp microelectrodes. Furthermore, noradrenaline did not elicit normal increases in lymphatic vessel tone when maximal constriction was reduced to 29.4 ± 4.9% of control in the presence of 20 nmol l(-1) nifedipine. Transcripts for the L-type calcium channel gene CACNA1C were consistently detected from human thoracic duct samples examined and the CaV1.2 protein was localized by immunoreactivity to lymphatic smooth muscle cells. While human lymphatics ex vivo were highly sensitive to nifedipine, this was not apparent in vivo when nifedipine was compared to placebo in a randomized, double-blinded clinical trial: conversely, lymphatic vessel contraction frequency was increased and refill time was faster despite all subjects achieving target nifedipine plasma concentrations. We conclude that human lymphatic vessels are highly sensitive to nifedipine in vitro but that care must be taken when extrapolating in vitro observations of lymphatic vessel function to the clinical situation, as similar changes in lymphatic function were not evident in our clinical trial comparing nifedipine treatment to placebo.</AbstractText>
<CopyrightInformation>© 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Telinius</LastName>
<ForeName>Niklas</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark Department of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark telinius@me.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mohanakumar</LastName>
<ForeName>Sheyanth</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark Department of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Majgaard</LastName>
<ForeName>Jens</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kim</LastName>
<ForeName>Sukhan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pilegaard</LastName>
<ForeName>Hans</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pahle</LastName>
<ForeName>Einar</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, Viborg Hospital, Viborg, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nielsen</LastName>
<ForeName>Jørn</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, Viborg Hospital, Viborg, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>de Leval</LastName>
<ForeName>Marc</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>International Congenital Cardiac Centre, Harley Street Clinic, London, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Aalkjaer</LastName>
<ForeName>Christian</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hjortdal</LastName>
<ForeName>Vibeke</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Department of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boedtkjer</LastName>
<ForeName>Donna Briggs</ForeName>
<Initials>DB</Initials>
<AffiliationInfo><Affiliation>Department of Biomedicine, Aarhus University, Aarhus, Denmark Department of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016449">Randomized Controlled Trial</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>08</Month>
<Day>28</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Physiol</MedlineTA>
<NlmUniqueID>0266262</NlmUniqueID>
<ISSNLinking>0022-3751</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002121">Calcium Channel Blockers</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020746">Calcium Channels, L-Type</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>I9ZF7L6G2L</RegistryNumber>
<NameOfSubstance UI="D009543">Nifedipine</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
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</CommentsCorrectionsList>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002121" MajorTopicYN="N">Calcium Channel Blockers</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020746" MajorTopicYN="N">Calcium Channels, L-Type</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018592" MajorTopicYN="N">Cross-Over Studies</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName>
<QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008564" MajorTopicYN="N">Membrane Potentials</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009119" MajorTopicYN="N">Muscle Contraction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D032389" MajorTopicYN="N">Myocytes, Smooth Muscle</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009543" MajorTopicYN="N">Nifedipine</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013897" MajorTopicYN="N">Thoracic Duct</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D046509" MajorTopicYN="N">Tissue Culture Techniques</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">PMC4253471</OtherID>
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<Month>8</Month>
<Day>31</Day>
<Hour>6</Hour>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25172950</ArticleId>
<ArticleId IdType="pii">jphysiol.2014.276683</ArticleId>
<ArticleId IdType="doi">10.1113/jphysiol.2014.276683</ArticleId>
<ArticleId IdType="pmc">PMC4253471</ArticleId>
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<affiliations><list><country><li>Danemark</li>
<li>Oman</li>
<li>Royaume-Uni</li>
</country>
<region><li>Angleterre</li>
<li>Grand Londres</li>
</region>
<settlement><li>Londres</li>
</settlement>
</list>
<tree><country name="Oman"><noRegion><name sortKey="Telinius, Niklas" sort="Telinius, Niklas" uniqKey="Telinius N" first="Niklas" last="Telinius">Niklas Telinius</name>
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<country name="Danemark"><noRegion><name sortKey="Mohanakumar, Sheyanth" sort="Mohanakumar, Sheyanth" uniqKey="Mohanakumar S" first="Sheyanth" last="Mohanakumar">Sheyanth Mohanakumar</name>
</noRegion>
<name sortKey="Aalkjaer, Christian" sort="Aalkjaer, Christian" uniqKey="Aalkjaer C" first="Christian" last="Aalkjaer">Christian Aalkjaer</name>
<name sortKey="Boedtkjer, Donna Briggs" sort="Boedtkjer, Donna Briggs" uniqKey="Boedtkjer D" first="Donna Briggs" last="Boedtkjer">Donna Briggs Boedtkjer</name>
<name sortKey="Hjortdal, Vibeke" sort="Hjortdal, Vibeke" uniqKey="Hjortdal V" first="Vibeke" last="Hjortdal">Vibeke Hjortdal</name>
<name sortKey="Kim, Sukhan" sort="Kim, Sukhan" uniqKey="Kim S" first="Sukhan" last="Kim">Sukhan Kim</name>
<name sortKey="Majgaard, Jens" sort="Majgaard, Jens" uniqKey="Majgaard J" first="Jens" last="Majgaard">Jens Majgaard</name>
<name sortKey="Nielsen, J Rn" sort="Nielsen, J Rn" uniqKey="Nielsen J" first="J Rn" last="Nielsen">J Rn Nielsen</name>
<name sortKey="Pahle, Einar" sort="Pahle, Einar" uniqKey="Pahle E" first="Einar" last="Pahle">Einar Pahle</name>
<name sortKey="Pilegaard, Hans" sort="Pilegaard, Hans" uniqKey="Pilegaard H" first="Hans" last="Pilegaard">Hans Pilegaard</name>
</country>
<country name="Royaume-Uni"><region name="Angleterre"><name sortKey="De Leval, Marc" sort="De Leval, Marc" uniqKey="De Leval M" first="Marc" last="De Leval">Marc De Leval</name>
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Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.

Human lymphatic vessel contractile activity is inhibited in vitro but not in vivo by the calcium channel blocker nifedipine.

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