Document Detail


Lipopolysaccharide impairs endothelial nitric oxide synthesis in rat renal arteries.
MedLine Citation:
PMID:  10844619     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Impaired endothelium-dependent vasodilation may contribute to hypoperfusion and failure of abdominal organs, including the kidneys during endotoxin or septic shock. In this study, the short-term (2 h) effects of bacterial lipopolysaccharide (LPS) on endothelium-dependent vasodilation in rat renal and superior mesenteric arteries were documented. METHODS: Rat renal and mesenteric arteries were dissected and exposed in vitro to LPS for two hours. The effects of LPS on vascular reactivity were determined and compared with time-matched controls. Endothelial nitric oxide (NO) release was determined using an NO microsensor in adjacent vessel segments. RESULTS: LPS impaired maximal acetylcholine (ACh)-induced endothelium-dependent vasodilation in renal arteries (62.5 +/- 8.8% vs. 34.4 +/- 7.5% in controls and LPS-exposed arteries), but not in mesenteric arteries. LPS did not alter the sensitivity of renal arteries to exogenous NO. ACh-dependent vasodilation was abolished after blocking NO synthesis with 10-4 mol/L L-NA in control and LPS-incubated renal arteries. When compared with controls, NO release induced by ACh and the receptor-independent calcium ionophore A23187 was significantly decreased (P < 0.05) in LPS-exposed renal segments and was fully abolished in endothelium-denuded segments, indicating that LPS attenuated receptor-dependent as well as receptor-independent endothelial NO release. In contrast, ACh- and A23187-induced NO release was normal in LPS-exposed mesenteric arteries. CONCLUSIONS: These results indicate that LPS-induced selective impairment of ACh-induced endothelium-dependent relaxation in rat renal arteries is caused by decreased endothelial NO release. This may contribute to the propensity for acute renal failure during septic shock.
Authors:
H A Piepot; C Boer; A B Groeneveld; A A Van Lambalgen; P Sipkema
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Kidney international     Volume:  57     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-08-24     Completed Date:  2000-08-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2502-10     Citation Subset:  IM    
Affiliation:
Departments of Physiology, Anesthesiology, and Internal Medicine (Intensive Care Unit), Institute for Cardiovascular Research, Vrije Universiteit, Amsterdam, The Netherlands. piepot@physiol.med.vu.nl
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MeSH Terms
Descriptor/Qualifier:
Animals
Endothelium, Vascular / drug effects,  physiology
Enzyme Inhibitors / pharmacology
Lipopolysaccharides / pharmacology*
Male
Muscle, Smooth, Vascular / drug effects,  physiology
Nitric Oxide / physiology
Nitric Oxide Synthase / antagonists & inhibitors,  biosynthesis*
Nitric Oxide Synthase Type III
Nitroarginine / pharmacology
Rats
Rats, Wistar
Renal Artery / drug effects,  metabolism*,  physiology
Time Factors
Vasodilation / physiology
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Lipopolysaccharides; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat

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


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