%0 Journal Article
%T Altered calcium signaling in platelets from nitric oxide-deficient hypertensive rats
%A David Iy¨²
%A Noem¨ª M Atucha
%A Concepci¨®n Mart¨ªnez-Prieto
%A M Clara Ortiz
%A Joaqu¨ªn Garc¨ªa-Esta£¿
%J Cell Communication and Signaling
%D 2004
%I BioMed Central
%R 10.1186/1478-811x-2-1
%X Basal calcium levels were always elevated in the platelets of the L-NAME-treated rats, both in the presence and in the absence of extracellular calcium. The administration of thrombin in the absence and in the presence of extracellular calcium induced important elevations in calcium levels that were always of greater magnitude in the platelets of the L-NAME-treated rats than in those of the controls. The addition of calcium to thapsigargin-treated platelets produced a massive elevation in calcium levels in both groups that was significantly greater in the platelets obtained from the hypertensive rats than in those of the controls.It is concluded that the arterial hypertension induced by the reduction of nitric oxide alters the regulation of platelet calcium levels so that elevated baseline levels and calcium entry and mobilization are enhanced. This could be the result of direct or indirect effects of the lack of nitric oxide synthesis in platelets or in other tissues.Nitric oxide (NO) is a very important regulator of numerous biological functions, among them the control of vascular tone. The reduction of NO production, either by inhibiting its synthesis or in situations of endothelial dysfunction, leads to arterial hypertension which then affects hemostatic, vascular, renal, and cardiac function, among others [1-3]. Arterial hypertension is also a risk factor for developing thrombotic events, which is related to activation of blood platelets which then can interact easily with a damaged vascular endothelium. It is thought that the mechanism responsible for the activation of platelets in hypertension is related to an increased cytosolic calcium (Ca2+) level and to an enhanced sensitivity to agonists, but the mechanisms responsible for this increase in platelet Ca2+ are not known [4,5].It is well known that NO plays an important role in aggregation of platelets. In fact, platelets were one of the first cell types where the L-arginine-nitric oxide pathway was characte
%K arterial hypertension
%K fura-2
%K calcium
%K L-NAME
%K nitric oxide
%K thrombin
%K thapsigargin
%K ionomycin
%U http://www.biosignaling.com/content/2/1/1