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Article: Normalization of renal aquaporin-2 water channel expression by fosinopril, valsartan, and combination therapy in congestive heart failure: A new mechanism of action

TitleNormalization of renal aquaporin-2 water channel expression by fosinopril, valsartan, and combination therapy in congestive heart failure: A new mechanism of action
Authors
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 2004, v. 36 n. 3, p. 445-453 How to Cite?
AbstractThis study investigated the effect of fosinopril (Fos), valsartan (Val), and combination of both drugs (Fos + Val) on the cardiac and renal expression of aquaporin-1 (AQP1) and aquaporin-2 (AQP2) in congestive heart failure (CHF). A rat model of CHF was created by ligating the left anterior descending coronary artery to induce acute myocardial infarction (AMI). Rats were treated by Fos, Val, or Fos + Val for 4 weeks. In renal medulla and cortex, AMI was associated with 2.2- and 1.8-fold increase in AQP2 mRNA expression when compared with Sham-operated rats (medulla: 23.6 ± 2.8 vs. 52.3 ± 8.7%; P < 0.001; cortex: 19.4 ± 3.9 vs. 35.5 ± 7.1%; P < 0.05). All the treatment regimens were able to normalize AQP2 transcription in the renal medulla (Fos, 19.9 ± 4.9%; Val, 22.8 ± 4.9%; Fos + Val, 20.1 ± 5.1%; P = NS vs. Sham) and in the cortex (Fos, 21.2 ± 6. 7%; Val, 20.4 ± 6.0%; Fos + Val, 18.9 ± 7.5%; P = NS vs. Sham). Similarly, the AQP2 protein expression increased by 2.1-fold after CHF (P < 0.05), and was normalized by the treatment regimens (Sham, 0.57 ± 0.19%; CHF, 1.22 ± 0.45%; Fos, 0.39 ± 0.36%; Val, 0.46 ± 0.34%; Fos + Val, 0.36 ± 0.15%; all P < 0.05 vs. CHF). These treatment regimens also prevented the increase in body weight as found in untreated CHF rats (analysis of variance P < 0.05). The renal and cardiac AQP1 gene and protein expressions were unaltered in CHF or by medical therapy. There was no observed cardiac AQP2 expression in all the study groups. Treatment with Fos, Val, or combination therapy was effective in preventing the upregulation of renal AQP2 gene and protein expressions in CHF rats caused by AMI. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76499
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, CMen_HK
dc.contributor.authorWingHon Lai, Ken_HK
dc.contributor.authorLi, PSen_HK
dc.contributor.authorLam, KYen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:21:53Z-
dc.date.available2010-09-06T07:21:53Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2004, v. 36 n. 3, p. 445-453en_HK
dc.identifier.issn0022-2828en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76499-
dc.description.abstractThis study investigated the effect of fosinopril (Fos), valsartan (Val), and combination of both drugs (Fos + Val) on the cardiac and renal expression of aquaporin-1 (AQP1) and aquaporin-2 (AQP2) in congestive heart failure (CHF). A rat model of CHF was created by ligating the left anterior descending coronary artery to induce acute myocardial infarction (AMI). Rats were treated by Fos, Val, or Fos + Val for 4 weeks. In renal medulla and cortex, AMI was associated with 2.2- and 1.8-fold increase in AQP2 mRNA expression when compared with Sham-operated rats (medulla: 23.6 ± 2.8 vs. 52.3 ± 8.7%; P < 0.001; cortex: 19.4 ± 3.9 vs. 35.5 ± 7.1%; P < 0.05). All the treatment regimens were able to normalize AQP2 transcription in the renal medulla (Fos, 19.9 ± 4.9%; Val, 22.8 ± 4.9%; Fos + Val, 20.1 ± 5.1%; P = NS vs. Sham) and in the cortex (Fos, 21.2 ± 6. 7%; Val, 20.4 ± 6.0%; Fos + Val, 18.9 ± 7.5%; P = NS vs. Sham). Similarly, the AQP2 protein expression increased by 2.1-fold after CHF (P < 0.05), and was normalized by the treatment regimens (Sham, 0.57 ± 0.19%; CHF, 1.22 ± 0.45%; Fos, 0.39 ± 0.36%; Val, 0.46 ± 0.34%; Fos + Val, 0.36 ± 0.15%; all P < 0.05 vs. CHF). These treatment regimens also prevented the increase in body weight as found in untreated CHF rats (analysis of variance P < 0.05). The renal and cardiac AQP1 gene and protein expressions were unaltered in CHF or by medical therapy. There was no observed cardiac AQP2 expression in all the study groups. Treatment with Fos, Val, or combination therapy was effective in preventing the upregulation of renal AQP2 gene and protein expressions in CHF rats caused by AMI. © 2003 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_HK
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_HK
dc.subject.meshAdministration, Oralen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntihypertensive Agents - administration & dosageen_HK
dc.subject.meshAquaporin 2en_HK
dc.subject.meshAquaporins - biosynthesisen_HK
dc.subject.meshDrug Therapy, Combinationen_HK
dc.subject.meshFosinopril - administration & dosageen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshHeart Failure - drug therapy - etiology - metabolism - pathologyen_HK
dc.subject.meshKidney Cortex - metabolism - pathologyen_HK
dc.subject.meshKidney Medulla - metabolism - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMyocardial Infarction - complications - metabolism - pathologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshTetrazoles - administration & dosageen_HK
dc.subject.meshValine - administration & dosage - analogs & derivativesen_HK
dc.titleNormalization of renal aquaporin-2 water channel expression by fosinopril, valsartan, and combination therapy in congestive heart failure: A new mechanism of actionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2828&volume=36&spage=445&epage=453&date=2004&atitle=Normalization+of+renal+aquaporin-2+water+channel+expression+by+fosinopril,+valsartan,+and+combination+therapy+in+congestive+heart+failure:+a+new+mechanism+of+actionen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yjmcc.2004.01.002en_HK
dc.identifier.pmid15010283-
dc.identifier.scopuseid_2-s2.0-1542358797en_HK
dc.identifier.hkuros87309en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1542358797&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume36en_HK
dc.identifier.issue3en_HK
dc.identifier.spage445en_HK
dc.identifier.epage453en_HK
dc.identifier.isiWOS:000220463500016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYu, CM=7404976646en_HK
dc.identifier.scopusauthoridWingHon Lai, K=6503860178en_HK
dc.identifier.scopusauthoridLi, PS=55495106200en_HK
dc.identifier.scopusauthoridLam, KY=25936276200en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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