Effect of Dietary Salt Loading and High‐calcium Diet on Vascular Smooth Muscle Responses and Endothelium Function in Rats

Abstract

1. The present study examined the effects of concurrent manipulation of dietary calcium and salt on contractile responses of vascular smooth muscle (VSM) and endothelial function of aortic rings from Sprague-Dawley rats. 2. Salt loading enhanced the contractile response of the aortic rings to noradrenaline (NA), an effect that was blunted by a high calcium intake. 3. Removal of the endothelium and incubation of aortic rings in physiological salt solution containing methylene blue increased the sensitivity of the rings to NA. 4. The increase in the sensitivity of aortic rings induced by endothelium removal was more pronounced in aortic rings from salt-loaded rats. 5. Acetylcholine caused similar degrees of relaxation in all experimental groups, but the relaxation to histamine was smaller (P < 0.05) in salt-loaded rats than in other groups of rats; however, after removal of the endothelium, the contractile response to histamine was higher in salt-loaded rats. 6. The results indicate that the hypersensitivity of isolated aortic rings to agonists, as observed in salt-loaded rats, is due to altered responses of the VSM and not as a result of changes in the endothelium. In addition, salt loading tends to increase the synthesis of endothelium-dependent relaxing factor. The ability of salt loading to enhance the contractile responses of VSM to agonists can be prevented by supplementing the diet with high calcium.

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

“…In addition, the response of denuded rings to KCl, which induces voltageactivated calcium entry from the extracellular space, and to caffeine, which mobilizes calcium from the sarcoplasmic reticulum, was markedly higher in the HS than in NS group. An increased sensitivity of the vascular smooth muscle cell to vasoconstrictors, such as noradrenaline, was also previously described in rats fed a HS diet (1). It was also reported that vascular reactivity to PE and KCl is greater in endothelininfused rats, particularly when fed a 8% NaCl diet during 9 days, and this was associated with increases in calcium entry from the extracellular space (23).…”

“…In various strains of rat, a high salt (HS) diet is associated with changes in the reactivity of aortic rings. Many studies conducted in salt-loaded models have shown an increased contraction of vascular smooth muscle cells in response to agonists (1,14). In addition, relaxation evoked by acetylcholine (ACh) or sodium nitroprusside (SNP) was obliterated in aortic rings isolated from adult spontaneously hypertensive and Dalh-sensitive rats fed a 8% NaCl diet for 4 -8 wk (12,14,16).…”

“…In contrast, an enhanced influence of nitric oxide (NO) may have a major role in the lack of rise in blood pressure of sodiumresistant rats when fed a HS diet. In the Dahl-resistant strain (16) and more clearly in the Sprague-Dawley rats (18), N Gnitro-L-arginine methyl ester (L-NAME) or 1H- [1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one, a guanylate cyclase inhibitor, enhanced phenylephrine (PE) contraction, and to a greater extent in rats fed an HS than a normal salt (NS) diet. Taken together, these results favor an adaptive response of both the endothelium and the vascular smooth muscle cells to chronic HS intake in adult rats of resistant strains.…”

Effects of high sodium intake diet on the vascular reactivity to phenylephrine on rat isolated caudal and renal vascular beds: Endothelial modulation

“…Many studies showed that sodium overload results in changes in sympathetic reflexes (Miyajima and Bunag, 1985;Ferrari and Mark, 1987) and changes in vascular reactivity (Mulvany et al, 1978;Adegunloye and Sofola, 1997;Nishida et al, 1998;Lenda et al, 2000). Additionally, there are changes in cardiac structure (Lal et al, 2003), function (Simchon et al, 1991), and volume that result in an increased cardiac output.…”

“…There are changes in vascular reactivity (Mulvany et al, 1978;Adegunloye and Sofola, 1997;Nishida et al, 1998;Lenda et al, 2000), in sympathetic reflexes (Miyajima and Bunag, 1985;Ferrari and Mark, 1987), on calcium mobilization, in Na + , K + -ATPase activity (Obiefuna et al, 1991a;Li et al, 1994), on endogenous sodium pump ligands levels (Fedorova et al, 2001), and in the balance between blood volume and cardiac output (Simchon et al, 1991).…”