Attenuated store-operated Ca2+ entry underpins the dual inhibition of nitric oxide and EDHF-type relaxations by iodinated contrast media
Author(s) -
Silvia Fernandez-Rodriguez,
D. H. Edwards,
Ben B. Newton,
Tudor M. Griffith
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp239
Subject(s) - myograph , cyclopiazonic acid , chemistry , nitric oxide , pharmacology , iohexol , biophysics , endothelium , endoplasmic reticulum , iodixanol , vasodilation , biochemistry , medicine , endocrinology , biology , organic chemistry , radiology , renal function , contrast medium
Our objective was to investigate whether alterations in endothelial Ca(2+) homeostasis contribute to the clinical toxicity of iodinated radiographic contrast media (IRCM) by modulating nitric oxide (NO) production and the endothelium-derived hyperpolarizing factor (EDHF) phenomenon.
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