Open AccessHydroxy-Methylglutaryl–Coenzyme A Reductase Inhibition Promotes Endothelial Nitric Oxide Synthase Activation Through a Decrease in Caveolin Abundance
Author(s) -
Olivier Féron,
Chantal Dessy,
JeanPierre Desager,
JeanLuc Balligand
Publication year - 2001
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.103.1.113
Subject(s) - enos , atorvastatin , caveolin 1 , nitric oxide , endocrinology , medicine , nitric oxide synthase type iii , reductase , cholesterol , endothelium , nitric oxide synthase , endothelial dysfunction , hmg coa reductase , chemistry , biochemistry , enzyme
Hypercholesterolemia is causally associated with defects of endothelial nitric oxide (NO)-dependent vasodilation. Increased uptake of cholesterol by endothelial cells (ECs) upregulates the abundance of the structural protein caveolin-1 and impairs NO release through the stabilization of the inhibitory heterocomplex between caveolin-1 and endothelial NO synthase (eNOS). Therefore, we examined whether the hydroxy-methylglutaryl-coenzyme A reductase inhibitor atorvastatin modulates caveolin abundance, eNOS activity, and NO release through a reduction in endogenous cholesterol levels.
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