Document Detail


ERK1/2-mediated vasoconstriction normalizes wall stress in small mesenteric arteries during NOS inhibition in vivo.
MedLine Citation:
PMID:  12960678     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As in essential hypertension, chronic nitric-oxide synthase (NOS) inhibition leads to hypertrophic remodeling in conduit and muscular arteries and inward eutrophic remodeling in small resistance arteries with activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in both vessel types. The authors tested the hypothesis that this remodeling heterogeneity could be related to distinct vasoreactivity patterns in small and larger arteries, with a vessel-specific function of ERK1/2 signaling. Using intravital microscopy in rats we have demonstrated that acute NOS inhibition (l-NA injection, 100 mg/kg) produced vasoconstriction of small mesenteric arteries. Consequently, the calculated in vivo wall stress was not significantly modified, despite the local rise in pressure. This could explain the lack of vascular protein synthesis elevation in vivo, an early index of hypertrophy. Inhibition of ERK1/2 activation with PD98059 blunted mesenteric artery contractions. Femoral arteries did not contract and were thus submitted to an enhanced wall stress and underwent hypertrophic remodeling in chronic conditions. In conclusion, the heterogeneous vascular remodeling in the l-NAME model is associated with a heterogeneous vasoconstriction response to acute NOS inhibition. Indeed, in contrast to larger arteries, l-NA-induced vasoconstriction in small arteries normalized wall stress and prevented early signs of hypertrophy. The results also suggest that ERK1/2 is a signaling element in NOS inhibition-induced vasoconstriction of small arteries in vivo.
Authors:
Daphné Girardot; Bénédicte Demeilliers; Denis deBlois; Pierre Moreau
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  42     ISSN:  0160-2446     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-09-08     Completed Date:  2003-12-23     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  339-47     Citation Subset:  IM    
Affiliation:
Université de Montréal, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects
Male
Mesenteric Arteries / drug effects
Mitogen-Activated Protein Kinase 1 / physiology*
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases / physiology*
Models, Cardiovascular
Muscle, Smooth, Vascular / drug effects*
NG-Nitroarginine Methyl Ester / pharmacology*
Nitric Oxide Synthase / antagonists & inhibitors*
Rats
Rats, Wistar
Renin / blood
Vasoconstriction / physiology*
Chemical
Reg. No./Substance:
50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.23.15/Renin

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


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