PMID- 8039844
OWN - NLM
STAT- MEDLINE
DCOM- 19940825
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 24
IP  - 2
DP  - 1994 Aug
TI  - Role of angiotensin II in renal injury of deoxycorticosterone acetate-salt 
      hypertensive rats.
PG  - 195-204
AB  - 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.
FAU - Kim, S
AU  - Kim S
AD  - Department of Pharmacology, Osaka City University Medical School, Japan.
FAU - Ohta, K
AU  - Ohta K
FAU - Hamaguchi, A
AU  - Hamaguchi A
FAU - Omura, T
AU  - Omura T
FAU - Yukimura, T
AU  - Yukimura T
FAU - Miura, K
AU  - Miura K
FAU - Inada, Y
AU  - Inada Y
FAU - Wada, T
AU  - Wada T
FAU - Ishimura, Y
AU  - Ishimura Y
FAU - Chatani, F
AU  - Chatani F
AU  - et al.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Benzimidazoles)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tetrazoles)
RN  - 0 (Transforming Growth Factor beta)
RN  - 11128-99-7 (Angiotensin II)
RN  - 40GP35YQ49 (Desoxycorticosterone)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 69PN84IO1A (Enalapril)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.4.23.15 (Renin)
RN  - R85M2X0D68 (candesartan cilexetil)
SB  - IM
MH  - Angiotensin II/*physiology
MH  - Animals
MH  - Benzimidazoles/pharmacology
MH  - Biphenyl Compounds/pharmacology
MH  - Collagen/genetics
MH  - Desoxycorticosterone
MH  - Enalapril/pharmacology
MH  - Hypertension/*complications/metabolism
MH  - Kidney/pathology
MH  - Kidney Diseases/*etiology
MH  - Male
MH  - Organ Size/drug effects
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Wistar
MH  - Renin/blood/genetics
MH  - Sodium Chloride
MH  - *Tetrazoles
MH  - Transforming Growth Factor beta/genetics
EDAT- 1994/08/01 00:00
MHDA- 1994/08/01 00:01
CRDT- 1994/08/01 00:00
PHST- 1994/08/01 00:00 [pubmed]
PHST- 1994/08/01 00:01 [medline]
PHST- 1994/08/01 00:00 [entrez]
AID - 10.1161/01.hyp.24.2.195 [doi]
PST - ppublish
SO  - Hypertension. 1994 Aug;24(2):195-204. doi: 10.1161/01.hyp.24.2.195.