Role of K+-channels and hydrogen sulfide in the regulation of cerebral arteries in nephrectomized rats
DOI:
https://doi.org/10.33910/2687-1270-2021-2-1-88-95Keywords:
chronic kidney disease, nephrectomy, cerebral arteries, vasodilation, acetylcholine, NO, endothelium-derived hyperpolarizing factor (EDHF), H2S, K -channelsAbstract
Chronic renal failure is widespread. It disrupts the functional state of cerebral arteries, leads to cognitive impairment and an increased risk of ischemic stroke. The study investigated the role of the endothelium-derived hyperpolarizing factor (EDHF) mediated mechanism and H2S in endothelium-dependent dilatation of cerebral arteries in nephrectomized (NE) rats. The study explored the reactions of cerebral arteries with a diameter of 60–80 μm and ˂ 20 μm NE and sham-operated male Wistar rats to acetylcholine (ACh) as well as to ACh acting under an NO synthase inhibitor, cystathionine γ-lyase and blocking of Ca2+-activated K+-channels. The attenuation of ACh-induced dilatation of cerebral arteries in NE rats with L-NAME was lower than in the control group. In the small arteries of the control group of rats, blocking of Ca2+ -activated K+-channels was accompanied by a decrease in ACh-induced dilatation by 11.2 ± 0.7%, in NE rats — by 18.8 ± 1.3%. Inhibition of cystathionine-γ-lyase in small arteries of control rats weakened ACh-induced dilatation by 14 ± 0.9%, in NE rats — by 22.8 ± 1.6%. It was concluded that the impairment of ACh-induced dilatation of arteries in NE rats is caused by a deficiency (bioavailability decrease) of NO. In small arteries, part of endothelium-dependent dilatation is realized through the EDH-type mechanism; in NE rats, the role of this mechanism increases. H2S is involved in endothelium-dependent dilatation of small cerebral arteries in control and NE rats (in the latter, H2S is a more significant vasodilator).
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