Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors

• Type: Article in International Scientific Journal
• Date: 2013

Authors

Daniela Patinha (Author) Other; Angelica Fasching (Author) Other; Dora Pinho (Author) FMUP; Antonio Albino Teixeira (Author) FMUP; Manuela Morato (Author) FFUP; Fredrik Palm (Author) Other

Journal

The Journal is awaiting validation by the Administrative Services.

Title: AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY

Vol. 304

Pages: F614-F622

ISSN: 1931-857X

Indexing

ISI Web of Knowledge - 20 Citations

ISI Web of Science

Scopus - 22 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

CORDIS: Health sciences

Other information

Authenticus ID: P-002-04N

DOI: 10.1152/ajprenal.00285.2012

Abstract (EN): Patinha D, Fasching A, Pinho D, Albino-Teixeira A, Morato M, Palm F. Angiotensin II contributes to glomerular hyperfiltration in diabetic rats independently of adenosine type I receptors. Am J Physiol Renal Physiol 304: F614-F622, 2013. First published January 2, 2013; doi:10.1152/ajprenal.00285.2012.-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.

Language: English

Type (Professor's evaluation): Scientific

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No. of pages: 9