Ionizing radiation induces vascular diseases causing arterial hypertension. A number of vascular disorders are associated with abnormalities of endothelium-dependent relaxation. The aim of present study was to investigate the role of nitric oxide (NO) and endothelium-derived hyperpolarization factor (EDHF) in development of hypertension evoked by the ionizing radiation impact.

Using selective inhibitors of NO-synthase and voltage-gated Ê+-channels, witches contribute to EDHF action was shown that g-radiation reduces endothelium-dependent vasodilatation and this reduction associated with inhibition of NO synthesis/release but not EDHF. Selective blockade of myoendothelial gap junction show that EDHF-dependent component of endothelium-mediated vasodilatation may be realised due to the conducting of hyperpolarizing electrical signals from endothelial cells to underlying smooth muscle.

This research was supported by a Wellcome Trust Collaborative Research Initiative grant 055 168/Z/98/Z.