Regulation of ANG II receptor in hypertension: role of ANG II
Wang, D.H.; Yao, A.; Zhao, H.; DiPette, D.J.
American Journal of Physiology 271(1 Pt 2): H120-H125
1996
ISSN/ISBN: 0002-9513 PMID: 8760166 Document Number: 458966
To investigate the role of angiotensin II (ANG II) in the development of hypertension induced by reduced renal mass (RRM) and the gene expression of ANG II type 1 (AT-1) receptors in the remnant renal tissue, four groups of rats were given 1% NaCl in water and subjected to RRM, RRM + ramipril, RRM + losartan, or sham surgery (control). Tail-cuff systolic blood pressure was significantly higher in RRM rats than in the other three groups. Northern blot showed that AT-1 gene expression was significantly decreased in RRM, RRM + ramipril, or RRM + losartan vs. control. There was no significant difference among the three RRM groups. Renal transforming growth factor-beta-1 (TGF-beta-1) mRNA levels were increased threefold (P lt 0.05) in RRM, RRM + ramipril, and RRM + losartan vs. control. There was no significant difference among the three RRM groups. We conclude that the development of RRM hypertension is ANG II dependent but not mediated by AT-1 gene expression. RRM downregulates AT-1 mRNA and upregulates TGF-beta-1 mRNA in the remnant renal tissue, regardless of blood pressure or plasma levels of ANG II, suggesting that these gene responses are triggered by an effect of local injury.