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Angiotensin (Ang) II AT‐2‐receptor‐induced nitric oxide (NO) release sustains blood perfusion and oxygen availability in the post‐clip kidney of two‐kidney, one clip hypertensive (2K1C) rats
Author(s) -
Palm Fredrik,
Connors Stephanie G.,
Welch William J.,
Wilcox Christopher S.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a497-d
Subject(s) - kidney , medicine , renovascular hypertension , renal blood flow , perfusion , vasoconstriction , renal artery , blood pressure , endocrinology , hypoxia (environmental) , renal circulation , cardiology , chemistry , oxygen , organic chemistry
We have shown previously that acute ACE inhibition (ACEI) causes a paradoxical renal vasoconstriction and hypoxia selectively in the post‐clip kidney of 2K1C rats. Therefore, we studied the role of NO and Ang II AT‐2 receptors in mediating these changes to ACEI. Three weeks after left renal artery clipping, cortical blood flow (CBF; laser Doppler) and oxygen tension (pO 2 ; Clark‐type microelectrodes) were measured after acute iv doses of ACEI (enalaprilat; n=8), L‐NAME (with control of renal perfusion pressure) followed by ACEI (n=7) or AT‐2 receptor blockade ( PD123319 ) followed by ACEI (n=7). Post‐clip vs non‐clip kidneys had lower baseline pO 2 (34±1 vs 51±1 mmHg). ACEI selectively lowered CBF (−44±11%) and pO 2 (−9±2 mmHg) in the post‐clip kidney. L‐NAME lowered CBF and pO 2 in the post‐clip kidney (−58±7% and −14±2 mmHg) and prevented changes in these parameters with ACEI. AT‐2 receptor blockade did not alter blood pressure but decreased CBF and pO 2 in the post‐clip kidney (−33±6% and −12±3 mmHg) and prevented changes in these parameters with ACEI. In conclusion, Ang II‐induced NO release via AT‐2 receptor activation maintains CBF and oxygen availability in the post‐clip kidney in the 2K1C renovascular hypertensive rat model. This finding provides a novel mechanism for Ang II to counteract hypoxia in a kidney challenged with a functional renal artery restriction.