Document Detail

Role of endothelin and nitric oxide imbalance in the pathogenesis of hypoxia-induced arterial hypertension.
MedLine Citation:
PMID:  9648078     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: We have recently demonstrated that prolonged hypobaric hypoxia can lead to a hematocrit-independent sustained arterial hypertension (HTN) in genetically normotensive Sprague-Dawley rats. The rise in blood pressure in the hypoxic animals was accompanied by a marked but transient increase in plasma endothelin level. In addition, hypoxia has been shown to decrease nitric oxide (NO) production by cultured endothelial cells. This study was designed to test the hypothesis that hypoxia-induced HTN may be mediated by increased endothelin and/or decreased NO production. METHODS: Blood pressure, plasma endothelin and urinary NO metabolites (NOx)were monitored in rats during a 24-hour exposure to hypobaric hypoxia (air pressure = 390 mm Hg). The results were compared with hypoxia (air pressure = 390 mm Hg). The results were compared with those obtained in animals maintained under normoxic condition (control group). To test the possible role of excess endothelin and depressed NO production, the studies were repeated using subgroups of animals treated with either an endothelin receptor ET-A/B blocker (L-754,142) or L-arginine. RESULTS: The untreated hypoxic group exhibited a threefold rise in plasma endothelin and a threefold fall in urinary NOx, prior to the onset of HTN. Endothelin receptor blockade led to a further fall in urinary NOx excretion and failed to mitigate HTN. In contrast, L-arginine supplementation improved the urinary NOx excretion and prevented HTN. Neither therapy affected the hypoxia-induced erythrocytosis. CONCLUSIONS: We conclude that hypoxia-induced HTN is associated with depressed NO production and can be mitigated by L-arginine supplementation.
Z Ni; S Bemanian; S D Kivlighn; N D Vaziri
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Kidney international     Volume:  54     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-09-16     Completed Date:  1998-09-16     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  188-92     Citation Subset:  IM    
Department of Medicine, University of California, Irvine, USA.
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MeSH Terms
Acetamides / pharmacology
Anoxia / complications,  physiopathology*
Arginine / pharmacology
Blood Pressure / drug effects
Disease Models, Animal
Endothelins / biosynthesis,  metabolism*
Hypertension, Renal / etiology,  physiopathology*
Kidney / blood supply,  chemistry,  enzymology
Nitrates / urine
Nitric Oxide / biosynthesis,  metabolism*
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type III
Nitrites / urine
Rats, Sprague-Dawley
Receptor, Endothelin A
Receptor, Endothelin B
Receptors, Endothelin / antagonists & inhibitors
Renal Circulation / physiology
Reg. No./Substance:
0/Acetamides; 0/Endothelins; 0/L 754142; 0/Nitrates; 0/Nitrites; 0/Receptor, Endothelin A; 0/Receptor, Endothelin B; 0/Receptors, Endothelin; 10102-43-9/Nitric Oxide; 74-79-3/Arginine; EC Oxide Synthase; EC Oxide Synthase Type III; EC protein, rat

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

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