Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributor.authorAllen, Terri Jen
dc.contributor.authorCao, Zeminen
dc.contributor.authorYoussef, Sen
dc.contributor.authorHulthen, U Len
dc.contributor.authorCooper, Mark Een
dc.identifier.citationDiabetes; 46(10): 1612-8en
dc.description.abstractWe explored the relative roles of the suppression of angiotensin II and the prevention of bradykinin degradation in mediating the renoprotective effects of ACE inhibitors in experimental diabetic nephropathy. Over a 24-week period, we studied male Sprague-Dawley diabetic and control rats and Sprague-Dawley diabetic rats treated with the ACE inhibitor ramipril, the angiotensin II-AT1 receptor antagonist valsartan, the bradykinin-B2 receptor antagonist HOE 140 (icatibant), and a combination of ramipril and icatibant. Serial measurements of urinary albumin excretion, blood pressure, and glycated hemoglobin were performed monthly. After 6 months, the animals were killed for the measurement of kidney weight and the assessment of glomerular ultrastructure. Over 24 weeks, urinary albumin excretion showed a continuous rise in the untreated diabetic rats. Both ramipril and valsartan, which were equihypotensive, prevented the increase in urinary albumin excretion over the whole study period. Icatibant therapy did not attenuate the antialbuminuric effect of the ACE inhibitor, nor did it have any effect as the sole therapy. Diabetes was associated with increased glomerular basement membrane thickness, glomerular volume, and total mesangial volume. Both ACE inhibition and angiotensin II receptor antagonism attenuated the glomerular ultrastructural changes to a similar degree. Icatibant did not attenuate the effects of ramipril on glomerular morphology. ACE inhibitors and angiotensin II-AT1 receptor blockers appear to confer similar benefits in experimental diabetic nephropathy, and bradykinin-B2 receptor blockers do not influence this effect. These findings suggest that the blockade of angiotensin II is the major pathway responsible for renoprotection afforded by ACE inhibition in experimental diabetic nephropathy.en
dc.subject.otherAngiotensin II.chemistry.physiologyen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.therapeutic useen
dc.subject.otherBlood Pressureen
dc.subject.otherBradykinin.analogs & derivatives.chemistry.pharmacology.physiologyen
dc.subject.otherBradykinin Receptor Antagonistsen
dc.subject.otherDiabetes Mellitus, Experimental.pathology.physiopathologyen
dc.subject.otherDiabetic Nephropathies.etiology.prevention & controlen
dc.subject.otherKidney Glomerulus.ultrastructureen
dc.subject.otherOrgan Sizeen
dc.subject.otherRamipril.therapeutic useen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherTetrazoles.therapeutic useen
dc.subject.otherValine.analogs & derivatives.therapeutic useen
dc.titleRole of angiotensin II and bradykinin in experimental diabetic nephropathy. Functional and structural studies.en
dc.typeJournal Articleen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg West, Australiaen
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
Appears in Collections:Journal articles
Show simple item record

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.