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Article: The calcium ionophore A23187 induces endothelium-dependent contractions in femoral arteries from rats with streptozotocin-induced diabetes

TitleThe calcium ionophore A23187 induces endothelium-dependent contractions in femoral arteries from rats with streptozotocin-induced diabetes
Authors
KeywordsCyclooxygenase
Endothelium
Endothelium-dependent contractions
Endothelium-derived contracting factor(s)
Smooth muscle
Streptozotocin-induced diabetes
Thromboxane-prostanoid receptor
Issue Date2007
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2007, v. 150 n. 5, p. 624-632 How to Cite?
AbstractBackground and purpose: To study the importance of endothelium-derived contracting factors (EDCFs) in arteries of rats with type I diabetes. Experimental approach: Rat femoral arteries were collected four or twelve weeks after induction of diabetes with streptozotocin. Rings, with or without endothelium, were suspended in organ chambers for isometric tension measurement. COX protein levels were determined by Western blotting. Key results: Four weeks after the injection of streptozotocin, the endothelium-dependent relaxations (during contractions to phenylephrine) to A23817 were attenuated, but the endothelium-dependent contractions (quiescent preparations) to the ionophore were augmented. Indomethacin and S18886 prevented the endothelium-dependent contractions, while dazoxiben reduced them in rings from streptozotocin-treated rats, suggesting that thromboxane A 2, activating TP- receptors, is involved. Twelve weeks after the injection of streptozotocin, the changes in endothelium-dependent relaxations and contractions to A23187 were even more noticeable. The protein expression of COX-1 was increased in femoral arteries of the diabetic rats. Valeryl salicylate and SC560 inhibited the contractions, suggesting that the EDCFs are produced by COX-1. At that time, a combination of S18886 with EP1-blockers was required to abolish the contractions, suggesting that the EDCFs involved act at both TP- and EP-receptors. Rings without endothelium from streptozotocin-treated rats exhibited a reduced maximal contraction to potassium chloride and U46619, combined with hyper-responsiveness to the latter, suggesting that more prolonged diabetes also alters the responsiveness of vascular smooth muscle. Conclusion and Implications: The production of EDCFs is progressively increased in the course of type I diabetes. Eventually, the disease also damages vascular smooth muscle. © 2007 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80316
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShi, Yen_HK
dc.contributor.authorFeletou, Men_HK
dc.contributor.authorKu, DDen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:57Z-
dc.date.available2010-09-06T08:04:57Z-
dc.date.issued2007en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2007, v. 150 n. 5, p. 624-632en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80316-
dc.description.abstractBackground and purpose: To study the importance of endothelium-derived contracting factors (EDCFs) in arteries of rats with type I diabetes. Experimental approach: Rat femoral arteries were collected four or twelve weeks after induction of diabetes with streptozotocin. Rings, with or without endothelium, were suspended in organ chambers for isometric tension measurement. COX protein levels were determined by Western blotting. Key results: Four weeks after the injection of streptozotocin, the endothelium-dependent relaxations (during contractions to phenylephrine) to A23817 were attenuated, but the endothelium-dependent contractions (quiescent preparations) to the ionophore were augmented. Indomethacin and S18886 prevented the endothelium-dependent contractions, while dazoxiben reduced them in rings from streptozotocin-treated rats, suggesting that thromboxane A 2, activating TP- receptors, is involved. Twelve weeks after the injection of streptozotocin, the changes in endothelium-dependent relaxations and contractions to A23187 were even more noticeable. The protein expression of COX-1 was increased in femoral arteries of the diabetic rats. Valeryl salicylate and SC560 inhibited the contractions, suggesting that the EDCFs are produced by COX-1. At that time, a combination of S18886 with EP1-blockers was required to abolish the contractions, suggesting that the EDCFs involved act at both TP- and EP-receptors. Rings without endothelium from streptozotocin-treated rats exhibited a reduced maximal contraction to potassium chloride and U46619, combined with hyper-responsiveness to the latter, suggesting that more prolonged diabetes also alters the responsiveness of vascular smooth muscle. Conclusion and Implications: The production of EDCFs is progressively increased in the course of type I diabetes. Eventually, the disease also damages vascular smooth muscle. © 2007 Nature Publishing Group All rights reserved.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectCyclooxygenaseen_HK
dc.subjectEndotheliumen_HK
dc.subjectEndothelium-dependent contractionsen_HK
dc.subjectEndothelium-derived contracting factor(s)en_HK
dc.subjectSmooth muscleen_HK
dc.subjectStreptozotocin-induced diabetesen_HK
dc.subjectThromboxane-prostanoid receptoren_HK
dc.titleThe calcium ionophore A23187 induces endothelium-dependent contractions in femoral arteries from rats with streptozotocin-induced diabetesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=150&spage=624&epage=632&date=2007&atitle=The+calcium+ionophore+A23187+induces+endothelium-dependent+contractions+in+femoral+arteries+from+rats+with+streptozotocin-induced+diabetesen_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.bjp.0706999en_HK
dc.identifier.pmid17245370en_HK
dc.identifier.scopuseid_2-s2.0-33847616500en_HK
dc.identifier.hkuros136340en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847616500&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume150en_HK
dc.identifier.issue5en_HK
dc.identifier.spage624en_HK
dc.identifier.epage632en_HK
dc.identifier.isiWOS:000244715600012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridShi, Y=7404964959en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK
dc.identifier.scopusauthoridKu, DD=7103238220en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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