RGD Reference Report - Angiotensin II type 2 receptors and nitric oxide sustain oxygenation in the clipped kidney of early Goldblatt hypertensive rats. - Rat Genome Database

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Angiotensin II type 2 receptors and nitric oxide sustain oxygenation in the clipped kidney of early Goldblatt hypertensive rats.

Authors: Palm, F  Connors, SG  Mendonca, M  Welch, WJ  Wilcox, CS 
Citation: Palm F, etal., Hypertension. 2008 Feb;51(2):345-51. Epub 2007 Dec 24.
RGD ID: 6903868
Pubmed: PMID:18158356   (View Abstract at PubMed)
DOI: DOI:10.1161/HYPERTENSIONAHA.107.097832   (Journal Full-text)

Angiotensin-converting enzyme inhibitors (ACEIs) decrease the glomerular filtration rate and renal blood flow in the clipped kidneys of early 2-kidney, 1-clip Goldblatt hypertensive rats, but the consequences for oxygenation are unclear. We investigated the hypothesis that angiotensin II type 1 or angiotensin II type 2 receptors or NO synthase mediate renal oxygenation responses to ACEI. Three weeks after left renal artery clipping, kidney function, oxygen (O(2)) use, renal blood flow, renal cortical blood flow, and renal cortical oxygen tension (Po(2)) were measured after acute administration of an ACEI (enalaprilat) and after acute administration of ACEI following acute administration of an angiotensin II type 1 or angiotensin II type 2 receptor blocker (candesartan or PD-123,319) or an NO synthase blocker (N(G)-nitro-L-arginine methyl ester with control of renal perfusion pressure) and compared with mechanical reduction in renal perfusion pressure to the levels after ACEI. The basal renal cortical Po(2) of clipped kidneys was significantly lower than contralateral kidneys (35+/-1 versus 51+/-1 mm Hg; n=40 each). ACEI lowered renal venous Po(2), cortical Po(2), renal blood flow, glomerular filtration rate, and cortical blood flow and increased the renal vascular resistance in the clipped kidney, whereas mechanical reduction in renal perfusion pressure was ineffective. PD-123,319 and N(G)-nitro-L-arginine methyl ester, but not candesartan, reduced the Po(2) of clipped kidneys and blocked the fall in Po(2) with acute ACEI administration. In conclusion, oxygen availability in the clipped kidney is maintained by angiotensin II generation, angiotensin II type 2 receptors, and NO synthase. This discloses a novel mechanism whereby angiotensin can prevent hypoxia in a kidney challenged with a reduced perfusion pressure.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
AGTR2Humanrenovascular hypertension  ISOAgtr2 (Rattus norvegicus) RGD 
Agtr2Ratrenovascular hypertension  IMP  RGD 
Agtr2Mouserenovascular hypertension  ISOAgtr2 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Agtr2  (angiotensin II receptor, type 2)

Genes (Mus musculus)
Agtr2  (angiotensin II receptor, type 2)

Genes (Homo sapiens)
AGTR2  (angiotensin II receptor type 2)


Additional Information