[The endothelium-derived hyperpolarization factor as a reserve defence mechanism of vasodilatation under conditions of ionizing radiation].

ABSTRACT

The goal of this study was to determine the cellular mechanisms of vascular endothelial dysfunction in rats irradiated with gamma-rays. Acetylcholine (Ach)-induced relaxation of rat thoracic aorta rings was measured as a test of endothelial integrity and function. The data obtained allow suggest that endothelial function is impaired in aorta from g-irradiated rats mainly due to the loss of EDRF/NO-dependent, but not EDHF-dependent relaxation. It has been shown that r-irradiation reduced the Ach-induced NO-release measured as nitrite anion content. Experiments on isolated rat aortic smooth muscle cells using whole-cell patch clamp technique demonstrated that irradiation led to a significant decrease in outward potassium currents. However, gamma-ray irradiation was without effect on K(+)-current carried through apamine-sensitive channels while the current through charybdotoxin-sensitive channels was increased as compared to cells from control animals. The data suggest that EDHF is resistant to ionized radiation and may constitute a crucial reserve mechanism for maintenance of blood flow under radiation. Therefore, it is likely that the subsequent studies related to EDHF identification will be important for new drugs development and targeted pharmacological intervention at endothelium dysfunction in case of radiation impact.