Influence of Intestinal Barrier on Alleviating an Increase in Blood Pressure by Sodium Alginate Intake in 2-Kidney, 1-Clip Renovascular Hypertensive Rats

Abstract

Sodium alginate (SALG) is a substance derived from brown seaweed that has been shown to reduce blood pressure (BP). However, its effects on renovascular hypertension caused by 2-kidney, 1-clip (2K1C) are not yet clear. Previous research suggests that hypertensive rats have increased intestinal permeability, and that SALG improves the gut barrier in inflammatory bowel disease mouse models. Therefore, the goal of this study was to determine whether the antihypertensive effects of SALG involve the intestinal barrier in 2K1C rats. Rats were fed either a 1.0% SALG diet or a control diet for six weeks after being subjected to 2K1C surgery or a sham operation. The systolic BP was measured weekly, and the mean arterial BP was measured at the end of the study. Intestinal samples were taken for analysis, and plasma lipopolysaccharide (LPS) levels were measured. The results showed that BP in 2K1C rats was significantly higher than in SHAM rats when fed CTL, but not when fed SALG. The gut barrier in 2K1C rats was improved by SALG intake. Plasma LPS levels also differed depending on the animal model and diet. In conclusion, dietary SALG may alleviate 2K1C renovascular hypertension by altering the gut barrier.

Effect of Saccharina japonica Intake on Blood Pressure and Gut Microbiota Composition in Spontaneously Hypertensive Rats

“…A previous report showed that the administration of potassium alginate lowered BP in SHRs and induced changes in gut microbiota [ 10 ]. As well, we previously observed that the intake of sodium alginate lowered BP in 2K1C rats and restored intestinal barrier function [ 11 ]. Furthermore, it was reported that alginate, fucoidan, and laminaran, when administered separately, altered the gut microbiota in normotensive rats and modulated the concentration of metabolites in the intestines [ 10 , 12 , 13 , 14 ].…”

“…Alginate, one of the main components of SJ, has been observed to suppress BP elevation in SHRs or 2K1C rats, respectively [ 10 , 11 , 60 ]. It has been reported that promoting sodium excretion is a potential mechanism for the effect of potassium alginate ingestion in suppressing the increase in BP.…”

“…Additionally, fecal sodium excretion was found to be very small in comparison to urine excretion [ 7 ]. Recently, we proposed one of the mechanisms behind this, which is the restoration of intestinal barrier function in 2K1C rats, by having observed an alleviation in the decreases in gut tight junction protein expression and the number of goblet cells in 2K1C rats fed alginate [ 11 ]. Therefore, the intake of SJ containing alginate may attenuate a decrease in intestinal barrier function in SHRs.…”

Marine Compounds and Age-Related Diseases: The Path from Pre-Clinical Research to Approved Drugs for the Treatment of Cardiovascular Diseases and Diabetes

“…Hypertensive rat treatment with fucoidan resulted in a persistent reduction of high blood pressure, with mechanisms that might involve an endothelial-protective function mediated by the Akt-eNOS signalling pathway [78]. In addition, the algal polysaccharides alginate, in both potassium and sodium form, has established anti-hypertensive activity, as demonstrated in spontaneous and induced rat models of hypertension [79][80][81][82][83], both as a scaffold for potassium delivery [79] and as an active molecule [80][81][82][83]. This effect was associated with low cardiovascular and renal damage [81] and downregulation of heart failure markers [82], and is likely due to a modulation of the gut microbiota and an improvement of the gut barrier [82,83] (Table 1).…”

“…In addition, the algal polysaccharides alginate, in both potassium and sodium form, has established anti-hypertensive activity, as demonstrated in spontaneous and induced rat models of hypertension [79][80][81][82][83], both as a scaffold for potassium delivery [79] and as an active molecule [80][81][82][83]. This effect was associated with low cardiovascular and renal damage [81] and downregulation of heart failure markers [82], and is likely due to a modulation of the gut microbiota and an improvement of the gut barrier [82,83] (Table 1). ACAT-acyl-coenzyme A:cholesterol acyl-transferase; ACE-angiotensin converting enzyme; COX1-cyclooxigenase 1; DOCA-deoxycorticosterone acetate; eNOS-endothelial nitric oxide synthase; NOX-4-NADPH oxydase 4; ICAM-1-intercellular adhesion molecule-1; LXR-β-liver X receptor beta; mPTP-mitochondrial permeability transition pore; PI3K-phosphatidyl inositol 3-kinase; NF-κB-nuclear factor kappa B; FGF-fibroblast growth factor; VEGF-vascular endothelial growth factor; BDNF-brain-derived neurotrophic factor; SREBP-2-sterol regulatory element-binding protein 2; PPARα-peroxisome proliferator activated receptor alpha; ERK-extracellular signal-regulated kinase; TXB2-thromboxane B2; VCAM-1-vascular cell adhesion molecule-1.…”