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Blood pressure, blood flow and oxygenation in the clipped kidney of long‐term Goldblatt hypertensive rats
Author(s) -
Palm Fredrik,
Onozato Maristela,
Welch William J,
Wilcox Christopher S
Publication year - 2009
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.23.1_supplement.803.3
Subject(s) - candesartan , medicine , renovascular hypertension , angiotensin ii , blood pressure , kidney , renin–angiotensin system , endocrinology , angiotensin ii receptor type 1 , renal blood flow , renal artery , afferent arterioles , cardiology , urology
Angiotensin II (Ang II) maintains blood flow (RBF) and oxygenation (pO 2 ) in the clipped kidney of early two‐kidney, one clip Goldblatt hypertensive rats (2K,1C). However, most cases of human renovascular disease are chronic. The involvement of Ang II declines whereas oxidative stress increases during progression of 2K,1C hypertension. We hypothesized that acute administration of drugs to inhibit reactive oxygen species (ROS; tempol), angiotensin converting enzyme (ACE; enalaprilat), Ang II type 1 or 2 receptors (AT 1 or AT 2 ; candesartan or PD‐123,319) lower mean arterial pressure (MAP), RBF and pO 2 in the clipped kidney of chronic 2K,1C. Twelve months after left renal artery clipping, MAP, RBF and pO 2 were measured after acute administration these drugs. MAP of 2K,1C was unchanged by PD123,319, reduced by ACE inhibition and AT1 blockade, and especially by tempol. Only tempol increased RBF and pO 2 in clipped kidneys. In conclusion, only tempol effectively reduces MAP and increases RBF and pO 2 in the clipped kidneys in the chronic model of Goldblatt hypertension. These beneficial renal effects of tempol can not be achieved by conventional interventions directed to the renin‐angiotensin system.