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Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
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2013 (English)In: American Journal of Physiology - Renal Physiology, ISSN 0363-6127, E-ISSN 1522-1466, Vol. 304, no 5, F614-F622 p.Article in journal (Refereed) Published
Abstract [en]

Increased angiotensin II (ANG II) or adenosine can potentiate each other in the regulation of renal hemodynamics and tubular function. Diabetes is characterized by hyperfiltration, yet the roles of ANG II and adenosine receptors for controlling baseline renal blood flow (RBF) or tubular Na+ handling in diabetes is presently unknown. Accordingly, the changes in their functions were investigated in control and 2-wk streptozotocin-diabetic rats after intrarenal infusion of the ANG II AT(1) receptor antagonist candesartan, the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), or their combination. Compared with controls, the baseline blood pressure, RBF, and renal vascular resistance (RVR) were similar in diabetics, whereas the glomerular filtration rate (GFR) and filtration fraction (FF) were increased. Candesartan, DPCPX, or the combination increased RBF and decreased RVR similarly in all groups. In controls, the GFR was increased by DPCPX, but in diabetics, it was decreased by candesartan. The FF was decreased by candesartan and DPCPX, independently. DPCPX caused the most pronounced increase in fractional Na+ excretion in both controls and diabetics, whereas candesartan or the combination only affected fractional Li+ excretion in diabetics. These results suggest that RBF, via a unifying mechanism, and tubular function are under strict tonic control of both ANG II and adenosine in both control and diabetic kidneys. Furthermore, increased vascular AT(1) receptor activity is a contribution to diabetes-induced hyperfiltration independent of any effect of adenosine A(1) receptors.

Place, publisher, year, edition, pages
2013. Vol. 304, no 5, F614-F622 p.
Keyword [en]
AT(1) receptors, A(1) receptors, tubular function, Na+ handling, diabetes
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-197629DOI: 10.1152/ajprenal.00285.2012ISI: 000315679500017OAI: oai:DiVA.org:uu-197629DiVA: diva2:614030
Note

Alternative ISSN: 1931-857X reported in WoS/ISI.

Available from: 2013-04-03 Created: 2013-04-02 Last updated: 2017-12-06Bibliographically approved

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Fasching, AngelicaPalm, Fredrik

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