Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs.
Identifieur interne : 000260 ( Ncbi/Merge ); précédent : 000259; suivant : 000261Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs.
Auteurs : W. Bernhard [Allemagne] ; E. Bothe-Sandtfort ; H. Koop ; W. Cassel ; P. Von WichertSource :
- European journal of clinical investigation [ 0014-2972 ] ; 1989.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Peptide vasoactif intestinal, Poumon.
- pharmacologie : Chloroquine.
- Animaux, Clairance métabolique, Lignées consanguines de rats, Mâle, Perfusion, Poumon, Rats, Techniques in vitro, Transport biologique actif.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Vasoactive Intestinal Peptide.
- chemical , pharmacology : Chloroquine.
- drug effects : Biological Transport, Active, Lung.
- metabolism : Lung.
- Animals, In Vitro Techniques, Male, Metabolic Clearance Rate, Perfusion, Rats, Rats, Inbred Strains.
Abstract
The degradation of vasoactive intestinal peptide (VIP) was studied using an isolated perfused rat lung model. 125iodine labelled VIP (125I-VIP) was used as a tracer. VIP was cleared from the perfusate by a single lung passage up to concentrations of 1 nmol l-1. The clearance rate was decreased at higher concentrations of VIP. VIP was taken up by the lung tissue and the cleavage products were re-extruded into the perfusate. The time delay of re-extrusion was increased at starting concentrations of VIP exceeding 1 nmol l-1 and in the presence of the lysosomal inhibitor chloroquine. After a bolus of 9 pmol or 40 nmol 125I-VIP into the pulmonary artery catheter 6.3 pmol or 2920 pmol, respectively, were bound by the lung. Most of the radioactive material was extruded within 25 min and consisted of low molecular weight 125I-labelled degradation products. We conclude that the receptors for VIP in the alveolar capillaries are of high affinity and capacity to extract VIP from the circulation and that lysosomes may be involved in the degradation. The degradation products are of low molecular weight.
DOI: 10.1111/j.1365-2362.1989.tb00267.x
PubMed: 2515970
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Bothe-Sandtfort</name></author><author><name sortKey="Koop, H" sort="Koop, H" uniqKey="Koop H" first="H" last="Koop">H. Koop</name></author><author><name sortKey="Cassel, W" sort="Cassel, W" uniqKey="Cassel W" first="W" last="Cassel">W. Cassel</name></author><author><name sortKey="Von Wichert, P" sort="Von Wichert, P" uniqKey="Von Wichert P" first="P" last="Von Wichert">P. 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Bernhard</name><affiliation wicri:level="1"><nlm:affiliation>Department of Internal Medicine, Philipps-University of Marburg, FRG.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Internal Medicine, Philipps-University of Marburg</wicri:regionArea><wicri:noRegion>Philipps-University of Marburg</wicri:noRegion><wicri:noRegion>Philipps-University of Marburg</wicri:noRegion><wicri:noRegion>Philipps-University of Marburg</wicri:noRegion></affiliation></author><author><name sortKey="Bothe Sandtfort, E" sort="Bothe Sandtfort, E" uniqKey="Bothe Sandtfort E" first="E" last="Bothe-Sandtfort">E. Bothe-Sandtfort</name></author><author><name sortKey="Koop, H" sort="Koop, H" uniqKey="Koop H" first="H" last="Koop">H. Koop</name></author><author><name sortKey="Cassel, W" sort="Cassel, W" uniqKey="Cassel W" first="W" last="Cassel">W. Cassel</name></author><author><name sortKey="Von Wichert, P" sort="Von Wichert, P" uniqKey="Von Wichert P" first="P" last="Von Wichert">P. Von Wichert</name></author></analytic><series><title level="j">European journal of clinical investigation</title><idno type="ISSN">0014-2972</idno><imprint><date when="1989" type="published">1989</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Transport, Active (drug effects)</term><term>Chloroquine (pharmacology)</term><term>In Vitro Techniques</term><term>Lung (drug effects)</term><term>Lung (metabolism)</term><term>Male</term><term>Metabolic Clearance Rate</term><term>Perfusion</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Vasoactive Intestinal Peptide (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Chloroquine (pharmacologie)</term><term>Clairance métabolique</term><term>Lignées consanguines de rats</term><term>Mâle</term><term>Peptide vasoactif intestinal (métabolisme)</term><term>Perfusion</term><term>Poumon ()</term><term>Poumon (métabolisme)</term><term>Rats</term><term>Techniques in vitro</term><term>Transport biologique actif ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Vasoactive Intestinal Peptide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Biological Transport, Active</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Peptide vasoactif intestinal</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>In Vitro Techniques</term><term>Male</term><term>Metabolic Clearance Rate</term><term>Perfusion</term><term>Rats</term><term>Rats, Inbred Strains</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Clairance métabolique</term><term>Lignées consanguines de rats</term><term>Mâle</term><term>Perfusion</term><term>Poumon</term><term>Rats</term><term>Techniques in vitro</term><term>Transport biologique actif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The degradation of vasoactive intestinal peptide (VIP) was studied using an isolated perfused rat lung model. 125iodine labelled VIP (125I-VIP) was used as a tracer. VIP was cleared from the perfusate by a single lung passage up to concentrations of 1 nmol l-1. The clearance rate was decreased at higher concentrations of VIP. VIP was taken up by the lung tissue and the cleavage products were re-extruded into the perfusate. The time delay of re-extrusion was increased at starting concentrations of VIP exceeding 1 nmol l-1 and in the presence of the lysosomal inhibitor chloroquine. After a bolus of 9 pmol or 40 nmol 125I-VIP into the pulmonary artery catheter 6.3 pmol or 2920 pmol, respectively, were bound by the lung. Most of the radioactive material was extruded within 25 min and consisted of low molecular weight 125I-labelled degradation products. We conclude that the receptors for VIP in the alveolar capillaries are of high affinity and capacity to extract VIP from the circulation and that lysosomes may be involved in the degradation. The degradation products are of low molecular weight.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2515970</PMID><DateCompleted><Year>1990</Year><Month>03</Month><Day>26</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0014-2972</ISSN><JournalIssue CitedMedium="Print"><Volume>19</Volume><Issue>6</Issue><PubDate><Year>1989</Year><Month>Dec</Month></PubDate></JournalIssue><Title>European journal of clinical investigation</Title><ISOAbbreviation>Eur. J. Clin. Invest.</ISOAbbreviation></Journal><ArticleTitle>Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs.</ArticleTitle><Pagination><MedlinePgn>506-13</MedlinePgn></Pagination><Abstract><AbstractText>The degradation of vasoactive intestinal peptide (VIP) was studied using an isolated perfused rat lung model. 125iodine labelled VIP (125I-VIP) was used as a tracer. VIP was cleared from the perfusate by a single lung passage up to concentrations of 1 nmol l-1. The clearance rate was decreased at higher concentrations of VIP. VIP was taken up by the lung tissue and the cleavage products were re-extruded into the perfusate. The time delay of re-extrusion was increased at starting concentrations of VIP exceeding 1 nmol l-1 and in the presence of the lysosomal inhibitor chloroquine. After a bolus of 9 pmol or 40 nmol 125I-VIP into the pulmonary artery catheter 6.3 pmol or 2920 pmol, respectively, were bound by the lung. Most of the radioactive material was extruded within 25 min and consisted of low molecular weight 125I-labelled degradation products. We conclude that the receptors for VIP in the alveolar capillaries are of high affinity and capacity to extract VIP from the circulation and that lysosomes may be involved in the degradation. The degradation products are of low molecular weight.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bernhard</LastName><ForeName>W</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Philipps-University of Marburg, FRG.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bothe-Sandtfort</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Koop</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Cassel</LastName><ForeName>W</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Von Wichert</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Eur J Clin Invest</MedlineTA><NlmUniqueID>0245331</NlmUniqueID><ISSNLinking>0014-2972</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>37221-79-7</RegistryNumber><NameOfSubstance UI="D014660">Vasoactive Intestinal Peptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001693" MajorTopicYN="N">Biological Transport, Active</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008657" MajorTopicYN="N">Metabolic Clearance Rate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010477" MajorTopicYN="N">Perfusion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011919" MajorTopicYN="N">Rats, Inbred Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014660" MajorTopicYN="N">Vasoactive Intestinal Peptide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1989</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1989</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1989</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2515970</ArticleId><ArticleId IdType="doi">10.1111/j.1365-2362.1989.tb00267.x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Bothe Sandtfort, E" sort="Bothe Sandtfort, E" uniqKey="Bothe Sandtfort E" first="E" last="Bothe-Sandtfort">E. Bothe-Sandtfort</name><name sortKey="Cassel, W" sort="Cassel, W" uniqKey="Cassel W" first="W" last="Cassel">W. Cassel</name><name sortKey="Koop, H" sort="Koop, H" uniqKey="Koop H" first="H" last="Koop">H. Koop</name><name sortKey="Von Wichert, P" sort="Von Wichert, P" uniqKey="Von Wichert P" first="P" last="Von Wichert">P. Von Wichert</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Bernhard, W" sort="Bernhard, W" uniqKey="Bernhard W" first="W" last="Bernhard">W. Bernhard</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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