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Article: Endothelin-1 blockade prevents COX2 induction and TXA 2 production in the fructose hypertensive rat

TitleEndothelin-1 blockade prevents COX2 induction and TXA 2 production in the fructose hypertensive rat
Authors
Issue Date2007
PublisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
Citation
Canadian Journal Of Physiology And Pharmacology, 2007, v. 85 n. 3-4, p. 422-429 How to Cite?
AbstractFeeding rats with a high fructose diet results in insulin resistance and hypertension. Fructose-hypertensive rats (FHR) have increased vascular levels of endothelin-1 (ET-1) and thromboxane (TXA2). We have previously shown that chronic treatment with either the dual endothelin receptor blocker, bosentan, or the thromboxane synthase inhibitor, dazmegrel, prevented fructose-induced increases in blood pressure, suggesting that both ET-1 and TXA2 play important roles in the development of hyperinsulinemia/ insulin resistance-associated hypertension. In this study, we investigated the potential interrelationship between ET-1 and TXA2 in the development of fructose-induced hypertension in vivo. Male Wistar rats were fed on a high fructose diet for 9 weeks. Either bosentan or dazmegrel treatment (daily by oral gavage) was initiated 3 weeks after the start of fructose feeding for a total duration of 6 weeks. At the end of drug treatment, blood and aorta were collected from each animal. Plasma thromboxane B2 (TXB2), a stable TXA2 metabolite, increased significantly in FHR and was reduced to control level by both chronic bosentan and dazmegrel treatment. Protein expression of cyclooxygenase 2 (COX2) was elevated significantly in FHR aortas and treatment with bosentan and dazmegrel corrected these changes. These results indicate that the actions of ET-1 in the aorta of FHR may be mediated through COX2-derived TXA2. Bosentan may prevent the development of hypertension in fructose-fed rats through inhibition of COX2 induction and subsequently the reduction in plasma TXA2. © 2007 NRC Canada.
Persistent Identifierhttp://hdl.handle.net/10722/147247
ISSN
2015 Impact Factor: 1.704
2015 SCImago Journal Rankings: 0.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Jen_US
dc.contributor.authorTran, Len_US
dc.contributor.authorVasudevan, Hen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorYuen, VGen_US
dc.contributor.authorMcneill, JHen_US
dc.date.accessioned2012-05-29T06:01:01Z-
dc.date.available2012-05-29T06:01:01Z-
dc.date.issued2007en_US
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 2007, v. 85 n. 3-4, p. 422-429en_US
dc.identifier.issn0008-4212en_US
dc.identifier.urihttp://hdl.handle.net/10722/147247-
dc.description.abstractFeeding rats with a high fructose diet results in insulin resistance and hypertension. Fructose-hypertensive rats (FHR) have increased vascular levels of endothelin-1 (ET-1) and thromboxane (TXA2). We have previously shown that chronic treatment with either the dual endothelin receptor blocker, bosentan, or the thromboxane synthase inhibitor, dazmegrel, prevented fructose-induced increases in blood pressure, suggesting that both ET-1 and TXA2 play important roles in the development of hyperinsulinemia/ insulin resistance-associated hypertension. In this study, we investigated the potential interrelationship between ET-1 and TXA2 in the development of fructose-induced hypertension in vivo. Male Wistar rats were fed on a high fructose diet for 9 weeks. Either bosentan or dazmegrel treatment (daily by oral gavage) was initiated 3 weeks after the start of fructose feeding for a total duration of 6 weeks. At the end of drug treatment, blood and aorta were collected from each animal. Plasma thromboxane B2 (TXB2), a stable TXA2 metabolite, increased significantly in FHR and was reduced to control level by both chronic bosentan and dazmegrel treatment. Protein expression of cyclooxygenase 2 (COX2) was elevated significantly in FHR aortas and treatment with bosentan and dazmegrel corrected these changes. These results indicate that the actions of ET-1 in the aorta of FHR may be mediated through COX2-derived TXA2. Bosentan may prevent the development of hypertension in fructose-fed rats through inhibition of COX2 induction and subsequently the reduction in plasma TXA2. © 2007 NRC Canada.en_US
dc.languageengen_US
dc.publisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjppen_US
dc.relation.ispartofCanadian Journal of Physiology and Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshCyclooxygenase 2 - Metabolismen_US
dc.subject.meshEndothelin-1 - Antagonists & Inhibitorsen_US
dc.subject.meshFructoseen_US
dc.subject.meshHypertension - Chemically Induced - Metabolism - Physiopathologyen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshInsulin - Blooden_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReceptors, Endothelin - Antagonists & Inhibitorsen_US
dc.subject.meshReceptors, Thromboxane - Metabolismen_US
dc.subject.meshSulfonamides - Pharmacologyen_US
dc.subject.meshThromboxane A2 - Metabolismen_US
dc.subject.meshThromboxane B2 - Blooden_US
dc.subject.meshThromboxane-A Synthase - Antagonists & Inhibitorsen_US
dc.titleEndothelin-1 blockade prevents COX2 induction and TXA 2 production in the fructose hypertensive raten_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1139/Y06-088en_US
dc.identifier.pmid17612651-
dc.identifier.scopuseid_2-s2.0-34547872828en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34547872828&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume85en_US
dc.identifier.issue3-4en_US
dc.identifier.spage422en_US
dc.identifier.epage429en_US
dc.identifier.isiWOS:000248052300018-
dc.publisher.placeCanadaen_US

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