Abstract
The homeostasis of cytosolic calcium [Ca^2+^]~c~ in mammalian cells is a complex phenomenon, requiring the contribution of many cellular and extracellular systems. Nitric oxide (NO) acts on [Ca^2+^]~c~, although the mechanism of this action is unknown. We study the release and the uptake of Ca^2+^ in the endoplasmic reticulum and its capacitative entry in human lymphomonocytes in the presence of the NO donor Sβnitrosocysteine (CysNO) at low (16 ΞΌM) and at high (160 ΞΌM) concentrations by measuring the [Ca^2+^]~c~ by the Fura 2βAM method. Thapsigargin (TG), which inhibits sarcoβendoplasmic reticulum Ca^2+^βATPase (SERCA), and nifedipine (NIF), which blocks the Ca^2+^ release from intracellular stores, are used to clarify the effects of NO on calcium movements. In the absence of extracellular Ca^2+^, CysNO decreases basal [Ca^2+^]~c~, whereas TG increases it as the result of SERCA inhibition. This effect of TG diminishes in the presence of the NO donor. In the presence of extracellular Ca^2+^(capacitative entry conditions), CysNO does not influence Ca^2+^ entry but reduces the toxic effects of TG connected to the increase of [Ca^2+^]~c~ in these conditions. The effect of NIF is, up to a certain extent, similar to that of CysNO, although the mechanisms of action of the two agents do not seem related. We conclude that CysNO participates in [Ca^2+^]~c~ homeostasis by stimulating the movement of the ion from the cytosol to other compartments. Β© 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:35β40, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20211