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. 2016 Jul 21;17(7):1176.
doi: 10.3390/ijms17071176.

Protective Effect of Salicornia europaea Extracts on High Salt Intake-Induced Vascular Dysfunction and Hypertension

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Protective Effect of Salicornia europaea Extracts on High Salt Intake-Induced Vascular Dysfunction and Hypertension

Nisha Panth et al. Int J Mol Sci. .

Abstract

High salt intake causes and aggravates arterial hypertension and vascular dysfunction. We investigated the effect of Salicornia europaea extracts (SE) on vascular function and blood pressure. SE constituents were analyzed using high performance liquid chromatography, and SE's effect on vascular function was evaluated in isolated porcine coronary arteries. SE's vascular protective effect was also evaluated in vivo using normotensive and spontaneous hypertensive rats (SHRs). SE mainly contained sodium chloride (55.6%), 5-(hydroxymethyl)furfural, p-coumaric acid, and trans-ferulic acid. High sodium (160 mmol/L) induced vascular dysfunction; however, SE containing the same quantity of sodium did not cause vascular dysfunction. Among the compounds in SE, trans-ferulic acid accounts for the vascular protective effect. Normotensive rats fed a high-salt diet showed significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP), which decreased significantly in the SE-treated groups. In SHRs, high edible salt intake significantly increased SBP, DBP, and MAP, but SE intake was associated with a significantly lower MAP. Thus, SE did not induce vascular dysfunction, and trans-ferulic acid might be at least partly responsible for the vasoprotective effect of SE. Taken together, SE could be used as an alternative to purified salt to prevent and ameliorate hypertension.

Keywords: Salicornia europaea; blood pressure; hypertension; vascular dysfunction.

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Figures

Figure 1
Figure 1
HPLC profiles for Salicornia europaea extracts (SE) and three reference compounds: 5-(hydroxymethyl)furfural (1); p-coumaric acid (2); and trans-ferulic acid (3). Chromatograms were extracted at 305 nm. (A) chromatograms of SE; and (BD) HPLC profile and UV spectra of 5-(hydroxymethyl)furfural (1); p-coumaric acid (2); and trans-ferulic acid (3).
Figure 2
Figure 2
Relaxant responses to bradykinin in porcine coronary arteries following incubation for 18 h with a medium containing a high sodium concentration (160 mmol/L) or Salicornia europaea extracts (SE) at the concentration equivalent to 160 mmol/L sodium. Relaxant responses are expressed as the percentage of relaxation of the initial tone induced by U46619. Values are expressed as mean ± SEM from n = 6 to 10 experiments. Concentration-response curves were compared using two-way ANOVA. “*” stands for p < 0.05 vs. control.
Figure 3
Figure 3
Dose-dependent vasorelaxant effects of 5-(hydroxymethyl)furfural, p-coumaric acid, and trans-ferulic acid in porcine coronary arteries (A) and vasorelaxant responses to bradykinin in porcine coronary arteries following incubation for 18 h with a medium containing a high sodium concentration (160 mmol/L) in presence or absence of 5-(hydroxymethyl)furfural (0.1 mmol/L), p-coumaric acid (0.1 mmol/L), and trans-ferulic acid (0.1 mmol/L) (B) and pre-treated with L-NAME (an inhibitor of eNOS, 0.1 mmol/L) (C). Relaxant responses are expressed as the percentage of relaxation of the initial tone induced by U46619. Values are expressed as mean ± SEM from n = 8 to 10 experiments. Concentration-response curves were compared using two-way ANOVA. “*” stands for p < 0.05 vs. NaCl.
Figure 4
Figure 4
Body weight (A,B) and food consumption (C,D) were examined in spontaneously hypertensive rats (B,D) and Sprague–Dawley (A,C) rats fed high edible salt and Salicornia europaea extracts (SE) for six weeks. CTR–SD, control SD rat; HS–SD, high edible salt-fed SD rat (800 mg/kg/day); SE–SD, SE-fed SD rat (1400 mg/kg/day); CTR–SHR, control SHR; HS–SHR, high edible salt-fed SHR (800 mg/kg/day); SE–SHR, SE-fed SHR (1400 mg/kg/day). Values are expressed as mean ± SEM. “***” stands for p < 0.001 vs. week 0.
Figure 5
Figure 5
Effect of Salicornia europaea extracts (SE) on the systolic blood pressure (A); diastolic blood pressure (B); and mean arterial pressure (C) in a normotensive SD rat group (CTR–SD) compared with the values in a high edible salt-fed group (HS–SD, 800 mg/kg/day) and a group fed SE (SE–SD, 1400 mg/kg/day). Values are expressed as mean ± SEM. “*”, “**” and “***” stand for p < 0.05, p < 0.01, and p < 0.001 vs. CTR–SD, respectively. “#” stands for p < 0.05 vs. HS–SD.
Figure 6
Figure 6
Effect of Salicornia europaea extracts (SE) on the systolic blood pressure (A); diastolic blood pressure (B); and mean arterial pressure (C) in the spontaneous hypertensive rat group (CTR–SHR) compared to the values in the high edible salt fed group (HS–SHR, 800 mg/kg/day) and the SE group (SE–SHR, 1400 mg/kg/day). Values are expressed as mean ± SEM. “***” stands for p < 0.001 vs. CTR-SD. “##” and “###” stands for p < 0.01 and p < 0.001 vs. CTR–SHR respectively. “$” stands for p < 0.05 vs. HS–SHR.
Figure 6
Figure 6
Effect of Salicornia europaea extracts (SE) on the systolic blood pressure (A); diastolic blood pressure (B); and mean arterial pressure (C) in the spontaneous hypertensive rat group (CTR–SHR) compared to the values in the high edible salt fed group (HS–SHR, 800 mg/kg/day) and the SE group (SE–SHR, 1400 mg/kg/day). Values are expressed as mean ± SEM. “***” stands for p < 0.001 vs. CTR-SD. “##” and “###” stands for p < 0.01 and p < 0.001 vs. CTR–SHR respectively. “$” stands for p < 0.05 vs. HS–SHR.

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References

    1. Kearney P.M., Whelton M., Reynolds K., Muntner P., Whelton P.K., He J. Global burden of hypertension: Analysis of worldwide data. Lancet. 2005;365:217–223. doi: 10.1016/S0140-6736(05)70151-3. - DOI - PubMed
    1. World Health Organization . A Global Brief on Hypertension: Silent Killer, Global Public Health Crisis. WHO Press; Geneva, Switzerland: 2013.
    1. Carretero O.A., Oparil S. Essential hypertension. Part I: Definition and etiology. Circulation. 2000;101:329–335. doi: 10.1161/01.CIR.101.3.329. - DOI - PubMed
    1. Li M., McDermott R. Obesity, albuminuria, and γ-glutamyl transferase predict incidence of hypertension in indigenous Australians in rural and remote communities in northern Australia. J. Hypertens. 2015;33:704–709. doi: 10.1097/HJH.0000000000000462. - DOI - PMC - PubMed
    1. Choi H.Y., Park H.C., Ha S.K. Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction. Electrolyte Blood Press. 2015;13:7–16. doi: 10.5049/EBP.2015.13.1.7. - DOI - PMC - PubMed

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