Effect of adenosine receptor agonists on release of the nucleoside analogue [3H]formycin B from cultured smooth muscle DDT1 MF-2 cells.
Identifieur interne : 001711 ( PubMed/Checkpoint ); précédent : 001710; suivant : 001712Effect of adenosine receptor agonists on release of the nucleoside analogue [3H]formycin B from cultured smooth muscle DDT1 MF-2 cells.
Auteurs : S L Borgland [Canada] ; F E ParkinsonSource :
- European journal of pharmacology [ 0014-2999 ] ; 1998.
English descriptors
- KwdEn :
- Affinity Labels, Animals, Cell Line, Cricetinae, Cyclic AMP (biosynthesis), Formycins (metabolism), Male, Mesocricetus, Muscle, Smooth (cytology), Muscle, Smooth (drug effects), Muscle, Smooth (metabolism), Purinergic P1 Receptor Agonists, Purinergic P1 Receptor Antagonists, Thioinosine (analogs & derivatives), Thioinosine (metabolism), Vas Deferens (cytology), Vas Deferens (drug effects), Vas Deferens (metabolism).
- MESH :
- chemical , analogs & derivatives : Thioinosine.
- chemical , biosynthesis : Cyclic AMP.
- chemical , metabolism : Formycins, Thioinosine.
- chemical : Affinity Labels, Purinergic P1 Receptor Agonists, Purinergic P1 Receptor Antagonists.
- cytology : Muscle, Smooth, Vas Deferens.
- drug effects : Muscle, Smooth, Vas Deferens.
- metabolism : Muscle, Smooth, Vas Deferens.
- Animals, Cell Line, Cricetinae, Male, Mesocricetus.
Abstract
Adenosine has receptor-mediated effects in a variety of cell types and is predominantly formed from ATP by a series of nucleotidase reactions. Adenosine formed intracellularly can be released by bidirectional nucleoside transport processes to activate cell surface receptors. We examined whether stimulation of adenosine receptors has a regulatory effect on transporter-mediated nucleoside release. DDT1 MF-2 smooth muscle cells, which possess nitrobenzylthioinosine-sensitive (ES) transporters as well as both adenosine A1 and A2 receptors, were loaded with the metabolically stable nucleoside analogue [3H]formycin B. N6-cyclohexyladenosine (CHA), a selective adenosine A1 receptor agonist, produced a concentration-dependent inhibition of [3H]formycin B release with an IC50 value of 2.7 microM. Further investigation revealed CHA interacts directly with nucleoside transporters with a Ki value of 3.3 microM. Neither 5'-N-ethylcarboxamidoadenosine (NECA), a mixed adenosine A1 and A2 receptor agonist, nor CGS 21680, a selective adenosine A2A receptor agonist, affected nucleoside release. We conclude that release of the nucleoside formycin B from DDT1 MF-2 cells is not regulated by adenosine A1 or A2 receptor activation.
PubMed: 9652378
Affiliations:
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Adenosine formed intracellularly can be released by bidirectional nucleoside transport processes to activate cell surface receptors. We examined whether stimulation of adenosine receptors has a regulatory effect on transporter-mediated nucleoside release. DDT1 MF-2 smooth muscle cells, which possess nitrobenzylthioinosine-sensitive (ES) transporters as well as both adenosine A1 and A2 receptors, were loaded with the metabolically stable nucleoside analogue [3H]formycin B. N6-cyclohexyladenosine (CHA), a selective adenosine A1 receptor agonist, produced a concentration-dependent inhibition of [3H]formycin B release with an IC50 value of 2.7 microM. Further investigation revealed CHA interacts directly with nucleoside transporters with a Ki value of 3.3 microM. Neither 5'-N-ethylcarboxamidoadenosine (NECA), a mixed adenosine A1 and A2 receptor agonist, nor CGS 21680, a selective adenosine A2A receptor agonist, affected nucleoside release. We conclude that release of the nucleoside formycin B from DDT1 MF-2 cells is not regulated by adenosine A1 or A2 receptor activation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9652378</PMID><DateCreated><Year>1998</Year><Month>09</Month><Day>16</Day></DateCreated><DateCompleted><Year>1998</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0014-2999</ISSN><JournalIssue CitedMedium="Print"><Volume>346</Volume><Issue>2-3</Issue><PubDate><Year>1998</Year><Month>Apr</Month><Day>10</Day></PubDate></JournalIssue><Title>European journal of pharmacology</Title><ISOAbbreviation>Eur. J. Pharmacol.</ISOAbbreviation></Journal><ArticleTitle>Effect of adenosine receptor agonists on release of the nucleoside analogue [3H]formycin B from cultured smooth muscle DDT1 MF-2 cells.</ArticleTitle><Pagination><MedlinePgn>339-44</MedlinePgn></Pagination><Abstract><AbstractText>Adenosine has receptor-mediated effects in a variety of cell types and is predominantly formed from ATP by a series of nucleotidase reactions. Adenosine formed intracellularly can be released by bidirectional nucleoside transport processes to activate cell surface receptors. We examined whether stimulation of adenosine receptors has a regulatory effect on transporter-mediated nucleoside release. DDT1 MF-2 smooth muscle cells, which possess nitrobenzylthioinosine-sensitive (ES) transporters as well as both adenosine A1 and A2 receptors, were loaded with the metabolically stable nucleoside analogue [3H]formycin B. N6-cyclohexyladenosine (CHA), a selective adenosine A1 receptor agonist, produced a concentration-dependent inhibition of [3H]formycin B release with an IC50 value of 2.7 microM. Further investigation revealed CHA interacts directly with nucleoside transporters with a Ki value of 3.3 microM. Neither 5'-N-ethylcarboxamidoadenosine (NECA), a mixed adenosine A1 and A2 receptor agonist, nor CGS 21680, a selective adenosine A2A receptor agonist, affected nucleoside release. We conclude that release of the nucleoside formycin B from DDT1 MF-2 cells is not regulated by adenosine A1 or A2 receptor activation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Borgland</LastName><ForeName>S L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parkinson</LastName><ForeName>F E</ForeName><Initials>FE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Eur J Pharmacol</MedlineTA><NlmUniqueID>1254354</NlmUniqueID><ISSNLinking>0014-2999</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000345">Affinity 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AMP</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000345" MajorTopicYN="N">Affinity Labels</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006224" MajorTopicYN="N">Cricetinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000242" MajorTopicYN="N">Cyclic AMP</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005573" MajorTopicYN="N">Formycins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008647" MajorTopicYN="N">Mesocricetus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009130" MajorTopicYN="N">Muscle, Smooth</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058906" MajorTopicYN="Y">Purinergic P1 Receptor Agonists</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058915" MajorTopicYN="N">Purinergic P1 Receptor Antagonists</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013868" MajorTopicYN="N">Thioinosine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014649" MajorTopicYN="N">Vas Deferens</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>7</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>7</Month><Day>4</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>7</Month><Day>4</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9652378</ArticleId><ArticleId IdType="pii">S0014-2999(98)00069-7</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Manitoba</li></region><settlement><li>Winnipeg</li></settlement><orgName><li>Université du Manitoba</li></orgName></list><tree><noCountry><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name></noCountry><country name="Canada"><region name="Manitoba"><name sortKey="Borgland, S L" sort="Borgland, S L" uniqKey="Borgland S" first="S L" last="Borgland">S L Borgland</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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