Hypertension, Vol 24, 195-204, Copyright © 1994 by American Heart Association
S Kim, K Ohta, A Hamaguchi, T Omura, T Yukimura, K Miura, Y Inada, T Wada, Y Ishimura and F Chatani
To investigate the role of angiotensin II (Ang II) in hypertension- induced
tissue injury, we gave TCV-116 (1 mg/kg per day PO), a nonpeptide Ang II
type I receptor antagonist, or enalapril (10 mg/kg per day PO) to
deoxycorticosterone acetate (DOCA)-salt hypertensive rats for 3 weeks and
examined the effects on tissue mRNA levels for transforming growth
factor-beta 1 (TGF-beta 1) and extracellular matrix components. Tissue mRNA
levels were measured by Northern blot analysis. Renal mRNA levels for
TGF-beta 1; types I, III, and IV collagen; and fibronectin in DOCA-salt
hypertensive rats were increased by severalfold (P < .01) compared with
sham-operated rats. In the aorta of DOCA-salt hypertensive rats, TGF-beta 1
and fibronectin mRNA levels were increased, but types I, III, and IV
collagen mRNAs did not increase. In the heart, increased mRNA was found
only for fibronectin. Thus, these gene expressions are regulated in a
tissue-specific manner. TCV-116 or enalapril did not lower blood pressure
in DOCA-salt hypertensive rats. However, the increase in renal mRNAs for
TGF-beta 1 and extracellular matrix components in DOCA-salt hypertensive
rats was significantly inhibited by treatment with TCV-116 or enalapril,
which was associated with a significant decrease in urinary protein and
albumin excretions and histological improvement of renal lesions. In
contrast, in the aorta and heart these gene expressions were not affected
by TCV-116 or enalapril. Thus, local Ang II may contribute to renal injury
of DOCA-salt hypertension by stimulating the gene expression of TGF-beta 1
and extracellular matrix components.
ARTICLES
Role of angiotensin II in renal injury of deoxycorticosterone acetate- salt hypertensive rats
Department of Pharmacology, Osaka City University Medical School, Japan.
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