Hyperuricemia Attenuates Aortic Nitric Oxide Generation, through Inhibition of Arginine Transport, in Rats
Author(s) -
Idit F. Schwartz,
Ayelet Grupper,
Tamara Chernichovski,
Oren Hillel,
Anat Engel,
Doron Schwartz
Publication year - 2010
Publication title -
journal of vascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 74
eISSN - 1423-0135
pISSN - 1018-1172
DOI - 10.1159/000320356
Subject(s) - benzbromarone , endocrinology , medicine , hyperuricemia , allopurinol , enos , nitric oxide , arginine , arginase , chemistry , nitric oxide synthase , uric acid , biochemistry , amino acid
Hyperuricemia provokes endothelial dysfunction (ECD). Decreased endothelial nitric oxide synthase (eNOS) activity is an important source of ECD. Cationic amino acid transporter-1 (CAT-1) is the specific arginine transporter for eNOS. We hypothesize that hyperuricemia inhibits arginine uptake.
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