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Effect of nicotine on intracellular Ca2+ concentrations and nitric oxide release in coronary artery endothelial cells
Author(s) -
Rejali Ali Reza,
Rejali Maryam,
Zhang Lubo,
Yang Shumei
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a523-b
Subject(s) - nitric oxide , nicotine , intracellular , chemistry , endothelium , pharmacology , endothelial stem cell , medicine , endocrinology , biochemistry , in vitro , organic chemistry
Studies in both humans and animals have demonstrated that nicotine impairs endothelium‐dependent relaxation of arterioles. It has been suggested that plasma levels of nitric oxide are decreased following the infusion of nicotine. The present study tested the hypothesis that nicotine has direct effects on endothelial cells and causes decreases in intracellular Ca2+ concentrations and nitric oxide release. Bovine coronary artery endothelial cells at the fifth passage were cultured to 80% confluence. For the time course study, cells were treated with 10 μM nicotine from 5 min to 48 h. To determine the dose‐response, cells were treated with 0.01 – 30 μM nicotine for 24 h. Intracellular Ca2+ concentrations were measured with cells loaded with fura‐2. Nitric oxide in culture medium was measured by the chemiluminescence method. Short‐term nicotine treatment up to 60 min showed no effect on intracellular Ca2+ concentrations and nitric oxide release. However, nicotine treatment for 24 h inhibited ATP‐induced increases in intracellular Ca2+ concentrations and significantly decreased the maximal Ca2+ response from 187.4±13.2 to 115.0±7.3 nM. In accordance, nicotine treatment had no effect on nitric oxide release until 24 h. At 24 h treatment, nicotine (0.01 to 30 μM) produced dose‐dependent decreases in nitric oxide release. The results suggest that chronic nicotine exposure decreases intracellular Ca2+ concentrations and nitric oxide release in cultured coronary artery endothelial cells. (Supported in part by NIH grant S06GM073842)