Dysfunction of arteries and microcirculatory vessels in rats with metabolic syndrome caused by a diet high in fructose
DOI:
https://doi.org/10.33910/2687-1270-2022-3-4-500-507Keywords:
metabolic syndrome, laser Doppler flowmetry (LDF), endothelial dysfunction, fructose load, nitric oxideAbstract
We studied the initial changes in the cardiovascular system of young Wistar rats when modeling the metabolic syndrome using fructose load. The experimental group showed signs of metabolic syndrome: hyperglycemia, insulin resistance, dyslipidemia, increased activity of the sympathetic nervous system, and arterial hypertension. Changes in the mesenteric arteries were revealed: an increase in reactivity to phenylephrine and a weakening of acetylcholine-induced dilatation, which is explained by a decrease in endothelial NO production. This was compensated to some extent by increased production of endothelial hyperpolarizing factor, which realizes its effect through the activation of Ca2+-sensitive K+-channels of intermediate conduction. Arterial smooth muscle cells in rats showed changes induced by fructose load: inhibition of soluble guanylate cyclase. In the MCR skin of rats that received fructose load, perfusion remained at the level characteristic of rats in the control group, while an increase in neurogenic tone and a weakening of the endothelium-dependent tone of skin microvessels was found. A decrease in NO production in the MCR vessels was also shown, which is compensated by the production of other vasodilating factors by the endothelium.
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