Роль NO и H 2 S в регуляции тонуса церебральных сосудов при хронической болезни почек

Abstract

Chronic kidney disease (CKD) is a widely spread condition that is a risk factor for the development of cerebrovascular diseases and neurological complications. Currently the mechanisms by which CKD increases the risk of brain damage are poorly understood. In our study, NO- and H2S-mediated changes in the cellular and molecular mechanisms of cerebral artery tone regulation were investigated in male Wistar rats in vivo with a CKD model. CKD was modeled by removal of 5/6 renal tissue at 4 months of age. After 4 months, part of the parietal bone and the dura mater were removed, and the diameter of the arteries was measured under the action of blockers and signaling pathway inhibitors using a microscope. In nephrectomized rats, the reactions of cerebral arteries to the application of acetylcholine (AH) manifested mainly in the form of constriction, while vasodilation predominated in the control group. Sodium nitroprusside led to a dilatation of the arteries, the amplitude of which in rats with CKD was significantly lower compared to the control group. Methylene blue and glibenclamide in rats with CKD led to a slight weakening of reactions to ACh, while in control group rats, the dilatation of arteries was significantly reduced. The degree of dilatation of cerebral arteries on H2S in rats with CKD was significantly less compared to rats in the control group. Propargylglycine caused only slight changes in artery diameter of CKD rats, while in the control group the reaction to propargylglycines was statistically significant. We conclude that the CKD attenuates endothelium-dependent and endothelium-independent NO- and H2S-mediated dilator reactions in cerebral arteries.