[Effect of high-fat diet on the reactivity of internal carotid artery from the Wistar rats].

Abstract

One of the main causes of obesity, which leads, in particular, to cardiovascular problems, is the consumption of food with a high fat content, however, the effect of a high-fat diet (HFD) on the contractile properties of blood vessels and the mechanisms of this effect have not been sufficiently studied, and information on this issue obtained on the internal carotid arteries (ICA), through which blood predominantly flows to the brain, is lacking. The aim of the research was to study the effect of HFD on the dilator and constrictor properties of the ICA in Wistar rats.

Material and methods: The study was conducted on 22 male Wistar rats, which at the age of 6 weeks were randomly divided into 2 groups: control (n=10) receiving standard diet, and group (n=12) kept on HFD (50% of fats by energy). After 8 weeks of feeding, the animals were euthanized with ether, after which the was excised from each rat. The reactivity of the ICA segments was assessed in the isometric mode. In isolated segments of vessels pre-contracted with phenylephrine, dilation was induced using acetylcholine or sodium nitroprusside, before and after addition of NO synthase (L-NAME), cyclooxygenase (diclofenac) and K+ channel blocker (tetraethylammonium) inhibitor.

Results: It was shown that the contractile response to phenylephrine of the ICA segment of the HFD rats was slightly greater than that of the control animals, both in the absence of inhibitors and a blocker in the bath (1.2±0.3 and 0.8±0.2 mN, respectively) and in their presence, while these differences were not statistically significant. The response of arteries (pre-contracted with phenylephrine) to acetylcholine was biphasic, and the dilator phase of this ICA response of the HFD rats in the absence of a blocker and inhibitors was almost 3-fold less compared to the control, amounting to -8.0±1.5 vs -21.6±7.1% (p<0.05). L-NAME caused a significant decrease in the dilator response of the ICA to acetylcholine (up to -8.4±2.7%, p<0.05) only in the control animals. The constrictor phase of the ICA response to acetylcholine in the absence of the blocker and inhibitors was significantly less than the dilator phase, amounting to 9.1±3.2% in the control animals and 2.6±1.0% in the HFD rats (р<0.05). In the HFD rats, the addition of diclofenac resulted in a significant increase in the contractile response to acetylcholine from 2.5±0.9 to 5.6±1.7% (р<0.05). The magnitude of ICA dilator reaction in the HFD rats induced by sodium nitroprusside in the absence of the blocker and inhibitors was slightly lower than in the control animals, amounting to 139±24 and 174±37%, respectively (р>0.05).

Conclusion: Consumption of HFD leads to a significant decrease in endotheliumdependent dilation of the ICA due to a decrease in NO synthesis by the endothelium, as well as to a disruption in the synthesis of prostaglandins.