Регуляция тонуса артерий у крыс, длительно получавших высокосолевую диету

Abstract

A high salt diet leads to a decrease in vascular dilatation to agonists, but the vascular mechanisms involved in this process are not extensively studied. A group of male Wistar rats at the age of 3 months was transferred to a diet containing 8% NaCl (HS) for 3 months, while the second group received a diet with a standard salt content (0.34%) (NS). At the end of the experiment, the rats were euthanized and the abdominal aorta and superior mesenteric artery (SMA) were extracted. The vascular segments were placed in a myograph and the acetylcholine (ACh) -induced relaxation of the vascular segments previously contracted with phenylephrine - was measured. A high salt diet led to a weakening of the relaxation of SMA in a calcium-free solution. In response to ACh and sodium nitroprusside, a pronounced relaxation of the vascular segments was observed, while the ACh-induced vascular relaxation of HS rats had a lower amplitude. K+ -channel blockers (TEA, TRAM-34, and apamine) weakened ACh-induced relaxation of the SMA, but not the aorta. In the SMA of HS rats the decrease in relaxation under the action of K+ -channel blockers was more significant. Inhibition of production of endogenous H2S also led to a weakening of the relaxation of the SMA segments on ACh. In SMA of HS rats, the degree of weakening of ACh-induced relaxation against the background of propargylglycine was greater than in NS rats. The data obtained in the study shows that a long-term high salt diet leads to a decrease in agonist-induced relaxation of the aorta segments and SMA. The relaxation weakening of the aorta segments and SMA occurs due to a decrease in the production of NO by the endothelium. In the SMA of HS rats, the decrease in NO-mediated relaxation is partially compensated by an increased role of EDHF in ACh-induced relaxation. The results of the study also show that one of the EDHFs in rat SMA is H2S, the role of which in SMA relaxation increases in HS rats.