Regulation of angiotensin ii receptor gene expression in reduced
renal mass hypertension: role of angiotensin ii.
Wang, Donna H., Aqing Yao, Huawei Zhao, Donald J. Dipette.
Department of Internal Medicine, Hypertension and Vascular Research
Laboratories, University of Texas Medical Branch, Galveston, TX
77555
APStracts 2:0545H, 1995.
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 (AT1) receptors in the remnant renal
tissue, four groups of rats were given 1% NaCl water and subjected
to: RRM, RRM plus ramipril, RRM plus losartan or sham surgery
(control). Tailcuff systolic blood pressure was significantly higher
in RRM rats than other three groups. Northern blot showed that AT1
gene expression was significantly decreased in RRM, RRM plus ramipril
or losartan vs control. There was no significant difference between
three RRM groups. Renal transforming growth factor-[beta]1 (TGF
-[beta]1) mRNA levels were increased by three-fold (p<0.05) in
RRM, RRM plus ramipril or losartan vs control. There was no
significant difference between three RRM groups. We conclude that the
development of RRM hypertension is Ang II-dependent but not mediated
by AT1 gene expression. RRM downregulates AT1 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.
Received 14 August 1995; accepted in final form 17 November 1995
APS Manuscript Number H767-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95