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

• Published in: Journal of evolutionary biochemistry and physiology 2021, Vol.57 (1), p.145-155
• Main Authors: Lobov, G. I., Ivanova, G. T.
• Format: Article
• Language: English
• Subjects: Animal Physiology; Biochemistry; Biomedical and Life Sciences; Evolutionary Biology; Experimental Papers; Life Sciences
• ISSN: 0022-0930; 1608-3202
• DOI: 10.1134/S0022093021010142

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 (H 2 S) 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 H 2 S, the role of which in SMA relaxation increases in HS rats.