Document Detail


Effects of chronic hypoxia on renal renin gene expression in rats.
MedLine Citation:
PMID:  10607761     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The effects of hypoxia on renin secretion and renin gene expression have been controversial. In recent studies, we have demonstrated that acute hypoxia of 6 h duration caused a marked stimulation of renin secretion and renal renin gene expression. This hypoxia-induced stimulation of the renin-angiotensin system might contribute, for example, to the progression of chronic renal failure and to the development of hypertension in the sleep-apnoea syndrome. For this reason, we were interested in the more chronic effects of hypoxia on renal renin gene expression and its possible regulation. METHODS: Male rats were exposed to chronic normobaric hypoxia (10% O(2)) for 2 and 4 weeks. Additional groups of rats were treated with an endothelin ET(A) receptor antagonist, LU135252, or a NO donor, molsidomine, respectively. Systolic blood pressure and right ventricular pressures were measured. Renal renin, endothelin-1 and endothelin-3 gene expression were quantitated using RNAase protection assays. RESULTS: During chronic hypoxia, haematocrit increased to 72+/-2%, and right ventricular pressure increased by a mean of 26 mmHg. Renal renin gene expression was halved during 4 weeks of chronic hypoxia. This decrease was reversed by endothelin receptor blockade (105 or 140% of baseline values after treatment for weeks 3-4 or 1-4). Furthermore, there was a trend of increasing renal endothelin-1 gene expression (to 173% of baseline values) after 4 weeks of hypoxia. Systolic blood pressure increased moderately during 4 weeks of chronic hypoxia from 129+/-2 to 150+/-4 mmHg. This blood pressure increase was higher in rats treated for 4 weeks with an endothelin receptor antagonist (196+/-11 mmHg). CONCLUSIONS: Chronic hypoxia (in contrast to acute hypoxia) suppresses renal renin gene expression. This inhibition presumably is mediated by endothelins.
Authors:
F Schweda; F C Blumberg; A Schweda; M Kammerl; S R Holmer; G A Riegger; M Pfeifer; B K Krämer
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  15     ISSN:  0931-0509     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-02-24     Completed Date:  2000-02-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  11-5     Citation Subset:  IM    
Affiliation:
Klinik und Poliklinik für Innere Medizin II, Klinikum der Universität Regensburg, Regensburg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / genetics*,  metabolism,  physiopathology
Blood Pressure / physiology
Chronic Disease
Endothelin-1 / genetics
Endothelin-3 / genetics
Gene Expression / drug effects
Kidney / metabolism*
Male
Molsidomine / pharmacology
Nitric Oxide Donors / pharmacology
Phenylpropionates / pharmacology
Pyrimidines / pharmacology
RNA, Messenger / genetics,  metabolism
Rats
Rats, Wistar
Receptors, Endothelin / antagonists & inhibitors
Renin / genetics*
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Endothelin-3; 0/LU 135252; 0/Nitric Oxide Donors; 0/Phenylpropionates; 0/Pyrimidines; 0/RNA, Messenger; 0/Receptors, Endothelin; 25717-80-0/Molsidomine; EC 3.4.23.15/Renin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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