uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • 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
Angiotensin II-nitric oxide interaction in the kidney
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.
2007 (English)In: Current opinion in nephrology and hypertension, ISSN 1062-4821, E-ISSN 1473-6543, Vol. 16, no 1, 46-51 p.Article, review/survey (Refereed) Published
Abstract [en]

PURPOSE OF REVIEW: The balance of angiotensin II and nitric oxide determines the sensitivity of the tubuloglomerular feedback mechanism, renal vascular resistance and filtration rate. Angiotensin II induces nitric oxide release, but the role of angiotensin II receptors here is not fully understood. Further, the angiotensin II-nitric oxide interaction can be modulated by reactive oxygen species. This review focuses on the angiotensin II-nitric oxide interaction and their modulation by reactive oxygen species in the control of renal blood flow. RECENT FINDINGS: Ideas about the role of angiotensin II type 1 and angiotensin II type 2 receptors are extended by the observation of angiotensin II type 1-mediated nitric oxide release with direct effects on vascular tone, tubuloglomerular feedback and sympathetic neurotransmission. Angiotensin receptors elicit disparate effects on intrarenal circulation. Angiotensin II-nitric oxide interactions are modulated by reactive oxygen species, as shown by angiotensin II type 1-mediated activation of superoxide and depression of antioxidant enzymes leading to reduced nitric oxide concentration - mechanisms that may be also important in angiotensin II-dependent hypertension. SUMMARY: Recent studies show that angiotensin II stimulates the nitric oxide system via angiotensin II type 1 and angiotensin II type 2 receptors, whereas receptors exert different effects on renal and medullary flow. The interaction via angiotensin II type 1 is modulated by reactive oxygen species.

Place, publisher, year, edition, pages
2007. Vol. 16, no 1, 46-51 p.
Keyword [en]
Angiotensin II/*metabolism, Animals, Kidney/*metabolism, Kidney Glomerulus/metabolism, Kidney Tubules/metabolism, Mice, Nitric Oxide/*metabolism, Reactive Oxygen Species/metabolism, Receptor; Angiotensin; Type 1/physiology, Receptor; Angiotensin; Type 2/physiology, Renal Circulation, Signal Transduction
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-13365DOI: 10.1097/MNH.0b013e328011a89bISI: 000243149100009PubMedID: 17143071OAI: oai:DiVA.org:uu-13365DiVA: diva2:41135
Available from: 2008-01-22 Created: 2008-01-22 Last updated: 2017-12-11Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=17143071&dopt=Citation

Authority records BETA

Persson, A Erik G

Search in DiVA

By author/editor
Persson, A Erik G
By organisation
Department of Medical Cell Biology
In the same journal
Current opinion in nephrology and hypertension
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 640 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • 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