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Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy
VITAMIN D ENHANCES NITRIC OXIDE PRODUCTION IN ENDOTHELIAL CELLS
Abstract number: P109
MOLINARI1 C, UBERTI1 F, GROSSINI1 E, VACCA1 G, INVERNIZZI1,3 M, CARDA2 S, CISARI1,2,3 C
1Department of Clinical and Experimental Medicine University of Eastern Piedmont, Novara
2Az. Ospedaliero-Universitaria Maggiore della Carit, Novara
3CRRF Mons. L. NOVARESE Rehabilitation Centre, Loc. Santuario del Trompone, Moncrivello (VC); (Italy)[email protected]
Aim:
Vitamin D (vitD) has usually been associated with the bone health. Recently, however, there has been evidence that vitD plays an important role in several tissues including myocardium and endothelium. For example, vitD deficiency seems to predispose to a number of cardiovascular diseases (Zittermann A, Prog Biophys Mol Biol, 92:39,2006). This research was planned to test the hypothesis that vitD plays a role in nitric oxide (NO) production within endothelial cells cultures.
Methods:
Human umbilical vein endothelial cells (HUVEC) cultures were used. Cells were treated with vitamin D3 (1-alpha,25-dihydroxycholecalciferol at various concentrations (10 pM, 100 pM, 1 nM, 10 nM, 100 nM), and at different times of administration (30s, 60s, 180s). NO production was determined by means of Griess method.
Results:
When applied to HUVEC cultures, vitD caused a significant dose-dependent increase in NO production. The most relevant response was obtained with a vitD concentration ranging from 1 to 10 nM (+975%; p<0.05). As regards the time course of the response, 60s administration appears to induce the greatest response. Administration of the vehicle alone to HUVEC cells, induced a very limited response (+5%) in NO production.
Conclusion:
vitD can induce an increase in NO production in endothelial cells. This finding add new information about the increasing importance of this hormone in the complex cardioprotective mechanisms that maintain cardiovascular health.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :P109