Open AccessExpression of Inducible Nitric Oxide Synthase Depresses β-Adrenergic–Stimulated Calcium Release From the Sarcoplasmic Reticulum in Intact Ventricular Myocytes
Author(s) -
Mark T. Ziolo,
Hideki Katoh,
Donald M. Bers
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/hc4901.100379
Subject(s) - forskolin , medicine , endocrinology , myocyte , ryanodine receptor , nitric oxide synthase , endoplasmic reticulum , nitric oxide , stimulation , chemistry , calcium , biology , microbiology and biotechnology
beta-adrenergic hyporesponsiveness in many cardiomyopathies is linked to expression of inducible nitric oxide synthase (iNOS) and increased production of NO. The purpose of this study was to examine whether iNOS expression alters the function of the sarcoplasmic reticulum (SR) Ca(2+) release channel (ryanodine receptor, RyR) during beta-adrenergic stimulation.
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