Regulation of Renin Gene Expression in Hypertensive Rats

A carboxy terminal renin complementary DNA (cDNA) clone from rat kidney was isolated, characterized, and used as a probe for renin messenger RNA (mRNA) quantification in normotensive and hypertensive rats. RNA blotting analysis detected renin mRNA in control kidney and brain. Deoxycorticosterone ace...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1988-10, Vol.12 (4), p.405-410
Main Authors: MAKRIDES, SAVVAS C, MULINARI, ROGERIO, ZANNIS, VASSILIS I, GAVRAS, HARALAMBOS
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Arterial hypertension. Arterial hypotension
Base Sequence
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Desoxycorticosterone - pharmacology
DNA - analysis
Experimental diseases
Gene Expression Regulation
Hypertension - genetics
Hypertension - metabolism
Male
Medical sciences
Molecular Sequence Data
Rats
Rats, Inbred Strains
Renin - genetics
RNA, Messenger - analysis
Sodium Chloride - pharmacology
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Summary:A carboxy terminal renin complementary DNA (cDNA) clone from rat kidney was isolated, characterized, and used as a probe for renin messenger RNA (mRNA) quantification in normotensive and hypertensive rats. RNA blotting analysis detected renin mRNA in control kidney and brain. Deoxycorticosterone acetate (DOCA) and high salt (1 %) treatment of experimental gnimnls resulted in a greater than 95% decrease in the content of renin mRNA in the kidney, as compared with values in control rats receiving 0.4% NaCl in their diet. In contrast, high salt (1%) treatment alone caused only a twofold decrease in kidney renin mRNA content, as compared with values in controls. DOCA and low salt (0.04%) or low salt (0.04%) treatment alone caused a 1.5-fold Increase in the kidney renin mRNA content, as compared with values in control rats. These results indicate that DOCA and salt have a synergistic effect in depressing renin mRNA levels in kidney. Clipping of the left renal artery caused a threefold increase in the steady state level of renin mRNA in the iscbemic kidney and a 0.5-fold decrease in the hypertrophied kidney. The data are consistent with the hypothesis that blood pressure and other stimuli regulate the expression of the renin gene in vivo.
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.12.4.405