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Article: Effects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuria

TitleEffects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuria
Authors
Issue Date2002
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394
Citation
Diabetes/Metabolism Research And Reviews, 2002, v. 18 n. 1, p. 71-76 How to Cite?
AbstractBackground. Microalbuminuria is associated with dysfunction of the vascular endothelium in patients with diabetes mellitus. The objective of the present study was to determine whether treatment with losartan at a dose sufficient to lower urinary albumin excretion was accompanied by an improvement in endothelial function in type 2 diabetic patients with microalbuminuria. Methods. Endothelial function was measured in 80 type 2 diabetic patients with microalbuminuria and 68 non-diabetic controls using high-resolution vascular ultrasound. The diabetic patients were randomised to receive either losartan 50 mg daily or placebo in a 6-month double-blind study. Urinary albumin excretion and endothelial function were assessed at baseline, 3 and 6 months. Results. Both endothelium-dependent (p < 0.01) and -independent vasodilation (p < 0.01) were significantly impaired in diabetic patients with or without history of hypertension compared to the non-diabetic controls. At baseline, the losartan- and placebo-treated groups were comparable in their clinical characteristics. Blood pressure did not change significantly in either group throughout the study. Urinary mean albumin excretion rate (MAER) decreased in the losartan-treated group (p < 0.01) whereas an increase was observed in the placebo group (p < 0.05). At 6 months, the losartan-treated group had significantly lower MAER than the placebo-treated group [54.5 (58.3) vs 78.5 (100.5) μg/min, p < 0.05; median (interquartile range)]. No significant differences were found in endothelium-dependent or -independent vasodilation. Conclusions. Type 2 diabetic patients with microalbuminuria have impaired endothelium-dependent and -independent vasodilation. Treatment with low-dose losartan is sufficient to reduce microalbuminuria in these patients without alteration in endothelial function and systemic blood pressure. Copyright © 2002 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162593
ISSN
2012 Impact Factor: 2.968
2015 SCImago Journal Rankings: 1.617
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_US
dc.contributor.authorChow, WSen_US
dc.contributor.authorAi, VHGen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2012-09-05T05:21:32Z-
dc.date.available2012-09-05T05:21:32Z-
dc.date.issued2002en_US
dc.identifier.citationDiabetes/Metabolism Research And Reviews, 2002, v. 18 n. 1, p. 71-76en_US
dc.identifier.issn1520-7552en_US
dc.identifier.urihttp://hdl.handle.net/10722/162593-
dc.description.abstractBackground. Microalbuminuria is associated with dysfunction of the vascular endothelium in patients with diabetes mellitus. The objective of the present study was to determine whether treatment with losartan at a dose sufficient to lower urinary albumin excretion was accompanied by an improvement in endothelial function in type 2 diabetic patients with microalbuminuria. Methods. Endothelial function was measured in 80 type 2 diabetic patients with microalbuminuria and 68 non-diabetic controls using high-resolution vascular ultrasound. The diabetic patients were randomised to receive either losartan 50 mg daily or placebo in a 6-month double-blind study. Urinary albumin excretion and endothelial function were assessed at baseline, 3 and 6 months. Results. Both endothelium-dependent (p < 0.01) and -independent vasodilation (p < 0.01) were significantly impaired in diabetic patients with or without history of hypertension compared to the non-diabetic controls. At baseline, the losartan- and placebo-treated groups were comparable in their clinical characteristics. Blood pressure did not change significantly in either group throughout the study. Urinary mean albumin excretion rate (MAER) decreased in the losartan-treated group (p < 0.01) whereas an increase was observed in the placebo group (p < 0.05). At 6 months, the losartan-treated group had significantly lower MAER than the placebo-treated group [54.5 (58.3) vs 78.5 (100.5) μg/min, p < 0.05; median (interquartile range)]. No significant differences were found in endothelium-dependent or -independent vasodilation. Conclusions. Type 2 diabetic patients with microalbuminuria have impaired endothelium-dependent and -independent vasodilation. Treatment with low-dose losartan is sufficient to reduce microalbuminuria in these patients without alteration in endothelial function and systemic blood pressure. Copyright © 2002 John Wiley & Sons, Ltd.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394en_US
dc.relation.ispartofDiabetes/Metabolism Research and Reviewsen_US
dc.subject.meshAdulten_US
dc.subject.meshAlbuminuria - Drug Therapyen_US
dc.subject.meshAngiotensin Receptor Antagonistsen_US
dc.subject.meshDiabetes Mellitus, Type 2 - Drug Therapy - Physiopathologyen_US
dc.subject.meshDouble-Blind Methoden_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLosartan - Therapeutic Useen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPlacebosen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleEffects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuriaen_US
dc.typeArticleen_US
dc.identifier.emailTan, KCB:kcbtan@hku.hken_US
dc.identifier.emailLam, KSL:ksllam@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/dmrr.255en_US
dc.identifier.pmid11921421-
dc.identifier.scopuseid_2-s2.0-0036200330en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036200330&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issue1en_US
dc.identifier.spage71en_US
dc.identifier.epage76en_US
dc.identifier.isiWOS:000174502000010-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTan, KCB=8082703100en_US
dc.identifier.scopusauthoridChow, WS=7402281153en_US
dc.identifier.scopusauthoridAi, VHG=6603342063en_US
dc.identifier.scopusauthoridLam, KSL=8082870600en_US

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