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Atopic dermatitis (AD) is a chronic, recurrent inflammatory skin disease, pathogenesis of which has not been fully recognised yet. Th1/ Th2 cells dysregulation, skin barrier defects and influence of environmental factors, including allergens and microbes seem to play an important role in the disease. Apart from infiltration from the inflammatory cells, the histological picture of skin lesions occurring in the course of the disease shows some oedema as well as the reparative processes appearing as fibrosis and angiogenesis which points to participation of factors contributing to endothelial permeability and the growth in pathomechanism of the disease. The vascular endothelial growth factor - VEGF, is a multifunctional proinflammatory cytokine which, 50 000 times stronger than histamine, increases the vascular endothelial permeability and plays the major role in angiogenesis. The role of such cytokine in the acute and chronic inflammatory response has been poorly recognised. Overproduction of VEGF in the skin and release into the bloodstream of patients suffering from AD has been pointed to, which suggest some role of this cytokine in the pathomechanism of AD.

It is known that NO is involved in a variety of physiological functions including the regulation of blood pressure. Dysregulation of L-arginine/NOS/NO biological activity occurs in blood hypertension. The present review will focus on a significance of NO in pathogenesis of essential hypertension.