Change in endothelial function in mesenteric arteries of sprague‐dawley rats fed a high salt diet

Abstract

A high salt diet in some species results in elevated arterial blood pressure and alterations in vascular smooth muscle responses to agonists. Weanling male Sprague‐Dawley rats were given either a high salt diet containing 8 % or a low salt diet of 0.4 % sodium chloride for a period of 4 weeks. At the end of the feeding period, tail systolic pressure was higher in the high salt than in low salt rats. The rats were then killed and the intestines removed. Vascular smooth muscle (VSM) responses were estimated from the changes in lumenal diameter of pressurised second order mesenteric resistance arteries. High salt diet resulted in enhanced VSM responses to noradrenaline. The vessels dilated in response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels from both high and low salt rats. However, vessels from high salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L‐NAME and the responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin. These results show that in Sprague‐Dawley rats, a high salt diet enhances the vasoconstriction in response to noradrenaline. The vasodilatory responses to acetylcholine were not significantly changed. However, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.

Upregulation of endothelium-derived hyperpolarizing factor compensates for the loss of nitric oxide in mesenteric arteries of dahl salt-sensitive hypertensive rats

“…Although Sofola et al 17 have previously reported that a high-salt diet augments EDHFlike relaxation, our present findings for the first time revealed the mechanism underlying the upregulation of EDHF in salt-induced hypertension. However, the mechanism by which a high-salt diet induces BKCa channel involvement in EDHF-mediated response could not be discerned from this results.…”

“…These results are in agreement with several previous studies demonstrating unaltered vasodilatory response to ACh in salt-induced hypertension despite the impairment of the NO pathway. 17,20 Although these results indicate that some compensatory mechanisms exist to maintain the vasodilatory response to ACh in salt-induced hypertension, few studies have shed light on the underlying mechanisms of this compensation.…”

“…11 Several mechanisms have been proposed to explain the reduced EDHF-mediated responses in mesenteric arteries of SHR: change in the expression profile of gap junctions, [12][13][14] increased activity of calcium-activated chloride channels 15 and reduced expression of small conductance calciumdependent potassium channels. 16 In contrast, Sofola et al 17 have reported that EDHF-like relaxation is upregulated in the mesenteric arteries of Sprague-Dawley rats fed a high-salt diet to compensate for the loss of NO. Upregulation of EDHF during hypertension has also been reported in renal arteries of SHR.…”

Decreased Renal Cytochrome P450 2C Enzymes and Impaired Vasodilation Are Associated With Angiotensin Salt-Sensitive Hypertension

“…[33][34][35][36] Lenda et al 33 reported that salt loading depressed acetylcholine-induced vasodilation of pial vessel, but Sifola et al 34 reported no difference in the acetylcholine responses in perfused mesenteric vessels. Unlike peripheral vascular beds, the renal vasculature maintains dilator responses, and the epithelium responds with changes in tubular transport that favor sodium excretion.…”

Chronic clofibrate administration prevents salineinduced endothelial dysfunction and oxidative stress in young Sprague-Dawley rats

“…In some studies, EDHF has been shown to compensate completely 8 for reduced nitric oxide activity and maintain normal endothelium dependent responses in aortic rings 26 and mesenteric vessels 27 of saline treated rats. However, other studies have shown reduced endothelium dependent relaxation responses in spino-trapezius vessels 5 and aortic rings.…”