liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals
Uppsala universitet, Institutionen för medicinsk cellbiologi.
Uppsala universitet, Institutionen för medicinsk cellbiologi.
Uppsala universitet, Institutionen för medicinsk cellbiologi.
Uppsala universitet, Institutionen för medicinsk cellbiologi.
Show others and affiliations
2008 (English)In: American Journal of Physiology - Renal Physiology, ISSN 0363-6127, E-ISSN 1522-1466, Vol. 294, no 2, 362-370 p.Article in journal (Refereed) Published
Abstract [en]

Hydronephrotic animals develop renal injury and hypertension, which is associated with an abnormal tubuloglomerular feedback (TGF). The TGF sensitivity is coupled to nitric oxide (NO) in the macula densa. The involvement of reduced NO availability in the development of hypertension in hydronephrosis was investigated. Hydronephrosis was induced by ureteral obstruction in young rats. Blood pressure and renal excretion were measured in adulthood, under different sodium conditions, and before and after chronic administration of either N-G- nitro-L-arginine methyl ester (L-NAME) or L-arginine. Blood samples for ADMA, SDMA, and L-arginine analysis were taken and the renal tissue was used for histology and determination of NO synthase (NOS) proteins. TGF characteristics were determined by stop-flow pressure technique before and after administration of 7-nitroindazole (7-NI) or L-arginine. Hydronephrotic animals developed salt-sensitive hypertension, which was associated with pressure natriuresis and diuresis. The blood pressure response to L-NAME was attenuated and L-arginine supplementation decreased blood pressure in hydronephrotic animals, but not in the controls. Under control conditions, reactivity and sensitivity of the TGF response were greater in the hydronephrotic group. 7-NI administration increased TGF reactivity and sensitivity in control animals, whereas, in hydronephrotic animals, neuronal NOS (nNOS) inhibition had no effect. L-Arginine attenuated TGF response more in hydronephrotic kidneys than in controls. The hydronephrotic animals displayed various degrees of histopathological changes. ADMA and SDMA levels were higher and the renal expressions of nNOS and endothelial NOS proteins were lower in animals with hydronephrosis. Reduced NO availability in the diseased kidney in hydronephrosis, and subsequent resetting of the TGF mechanism, plays an important role in the development of hypertension.

Place, publisher, year, edition, pages
2008. Vol. 294, no 2, 362-370 p.
Keyword [en]
ADMA, tubuloglomerular feedback, L-arginine, L-NAME, telemetry, blood pressure
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-99298DOI: 10.1152/ajprenal.00410.2007ISI: 000252744300010OAI: oai:DiVA.org:liu-99298DiVA: diva2:657206
Available from: 2008-03-28 Created: 2013-10-15 Last updated: 2017-12-06

Open Access in DiVA

No full text

Other links

Publisher's full text

Authority records BETA

Edlund, JennyLarsson, ErikPalm, FredrikPersson, A. Erik G.

Search in DiVA

By author/editor
Edlund, JennyLarsson, ErikPalm, FredrikPersson, A. Erik G.
In the same journal
American Journal of Physiology - Renal Physiology
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 39 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf