Regulation of ANG II receptor in hypertension: role of ANG II

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 in water and subjected to RRM, RRM+ ramipril, RRM+ lo...

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Published inThe American journal of physiology Vol. 271; no. 1 Pt 2; p. H120
Main Authors Wang, D H, Yao, A, Zhao, H, DiPette, D J
Format Journal Article
LanguageEnglish
Published United States 01.07.1996
Subjects
Angiotensin II - genetics
Angiotensin II - physiology
Angiotensin Receptor Antagonists
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals
Biphenyl Compounds - pharmacology
Gene Expression - drug effects
Hypertension - physiopathology
Imidazoles - pharmacology
Losartan
Male
Nephrectomy - methods
Ramipril - pharmacology
Rats
Rats, Wistar
Receptors, Angiotensin - metabolism
RNA, Messenger - metabolism
Tetrazoles - pharmacology
Transforming Growth Factor beta - genetics
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Summary: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 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 AT1 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 < 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 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.
ISSN:0002-9513
DOI:10.1152/ajpheart.1996.271.1.H120