Key result
H2S synthesis inhibition reduces cerebral arterial dilatation by ~23% in uremic rats vs. controls.
Why the study?
Chronic renal failure disrupts cerebral artery function, leading to cognitive impairment and increased ischemic stroke risk, but the roles of EDHF and H2S in cerebral artery dilation in this context are unclear.
Answers are grounded in this paper and cite their sources.
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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Lobov et al. (2021) studied Chronic kidney disease (uremia) (n=26). 5/6 nephrectomy vs. Sham operation was evaluated on Reduction in ACh-induced dilatation of small cerebral arteries upon inhibition of cystathionine-γ-lyase (H2S synthesis) (p=<0.01). In nephrectomized rats, inhibition of H2S synthesis reduced ACh-induced dilatation of small cerebral arteries by 22.8% compared to 14.0% in controls, indicating an increased compensatory role of H2S.
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