NO-dependent mechanism of vasodilation in pial arteries of nefrectomizedrats

Abstract

THE AIM: to study changes in the NO-mediated dilatation mechanism in the pial arteries of the brain of nephrectomized rats.MATERIALS AND METHODS: The study was conducted on Wistar-Kyoto rats. At 4 months of age, a two-stage nephrectomy was performed. After 3 months, the reaction of the arteries of the pial membrane of the brain to agonists and antagonists was investigated by in vivo microscopy (the diameter of the arteries was measured against the action of acetylcholine, sodium nitroprusside and methylene blue). Besides, the perfusion of the brain tissue was measured for subsequent calculations of the values of the components of the vascular tone.RESULTS: It was shown that the application of acetylcholine to the pial membrane led to a change in the diameter of the arteries. In nephrectomized rats under the action of acetylcholine, a significantly larger number of arteries in the constriction state was registered compared to the control group. The effect of sodium nitroprusside in the control group was accompanied by a dilatation of 100 % of the pial arteries; in the nephrectomized rat group, dilatation was detected in 83.2 ± 4.7 % of the arteries. When methylene blue was used in a group of nephrectomized rats, a smaller number of arteries in the constriction state was detected as compared to the control group.CONCLUSION: In nephrectomized rats, pronounced disorders of the NO-mediated mechanism of the pial arteries of the brain were found, leading to an increase in the endothelial component of the vascular tone. The endothelium of the pial arteries of nephrectomized rats produces less NO both spontaneously and when stimulated with acetylcholine. In nephrectomized rats, abnormalities in the signal cascade of NO →sGC → cGMP in the smooth muscle cells of the pial arteries were revealed, which is confirmed by their lesser ability to dilate to the use of exogenous NO.