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  • Patinha, DanielaUppsala universitet,Institutionen för medicinsk cellbiologi,Uppsala University, Sweden (författare)

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

  • Artikel/kapitelEngelska2013

Förlag, utgivningsår, omfång ...

  • American Physiological Society,2013
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:liu-90668
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-90668URI
  • https://doi.org/10.1152/ajprenal.00285.2012DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-197629URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Funding Agencies|Swedish Medical Research Council|994072XD-150431084014X-2553K2003-04X-03522-32|Swedish Society for Medical Research||National Institute of Diabetes and Digestive and Kidney Diseases|DK-077858|FCT||FEDER||POFC-COMPETE|PTDC/SAU-FCF/67764/2006SFRH/BD/43187/2008|
  • Alternative ISSN: 1931-857X reported in WoS/ISI.
  • 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.

Ämnesord och genrebeteckningar

  • AT(1) receptors
  • A(1) receptors
  • tubular function
  • Na+ handling
  • diabetes
  • TECHNOLOGY
  • TEKNIKVETENSKAP

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Fasching, AngelicaUppsala universitet,Institutionen för medicinsk cellbiologi,Uppsala University, Sweden(Swepub:uu)afa22979 (författare)
  • Pinho, DoraUniversity of Porto, Portugal (författare)
  • Albino-Teixeira, AntonioUniversity of Porto, Portugal (författare)
  • Morato, ManuelaUniversity of Porto, Portugal (författare)
  • Palm, Fredrik,1973-Uppsala universitet,Linköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet,Department of Medical Cell Biology, Uppsala University,Institutionen för medicinsk cellbiologi(Swepub:uu)fredpalm (författare)
  • Uppsala universitetInstitutionen för medicinsk cellbiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY: American Physiological Society304:5, s. F614-F6221931-857X1522-14660363-6127

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