Regulation of Arterial Tone in Rats Fed a Long-Term High-Salt Diet

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 high-salt diet containing 8% NaCl (HS) for 3 months, while the second group received a normal-salt 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 into a myograph, and the acetylcholine (ACh)-induced relaxation of the phenylephrine (PHE)-precontracted vascular segments was measured. A high-salt diet led to attenuate the relaxation of the 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 in HS rats showed a lower amplitude. Potassium channel blockers (TEA, TRAM-34, apamine) attenuated the ACh-induced relaxation of the SMA, but not the aorta. In the SMA of HS rats, a decrease in the relaxation under the effect of K+ channel blockers was more prominent. Inhibition of the production of endogenous hydrogen sulfide (H2S) also led to attenuate the ACh-induced relaxation of SMA segments. In SMA of HS rats, the degree of attenuation of the ACh-induced relaxation against the background of propargylglycine was larger than in NS rats. The data obtained in the study show that a long-term high-salt diet leads to a decrease in agonist-induced relaxation of the aortic segments and SMA due to a decrease in the production of NO by the endothelium. In the SMA of HS rats, a decrease in NO-mediated relaxation is partially compensated by the increasing role of EDHF in ACh-induced relaxation. The results of the study also show that one of the EDHFs in the rat SMA is H2S, the role of which in SMA relaxation increases in HS rats.