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

It was reported that the consumption of Saccharina japonica (SJ) lowers blood pressure (BP) in hypertensive rats. Hypertension is related to gut microbiota, and hypertensive patients develop dysbiosis. It was reported that the intake of dietary fiber and polysaccharides contained in SJ changes gut microbiota and increases short-chain fatty acids (SCFAs). The present study examined the effect of BP lowering by SJ in spontaneously hypertensive rats (SHRs) and observed changes in gut microbiota composition and SCFAs concentration. Male SHRs and Wistar Kyoto rats (WKYs) were fed a diet containing 5% SJ or a control diet for six weeks. We measured systolic BP (SBP) weekly, as well as mean arterial BP (MAP), the 16S rRNA gene, and SCFAs in the cecal contents at the end of the period. As a result, the intake of SJ significantly decreased SBP and MAP in SHRs. As well, it significantly changed the microbial diversity by altering the gut microbiota composition. Particularly, it increased the abundance of Bacteroides acidifaciens, which may be associated with the antihypertensive effect of SJ. Thus, SJ intake suppressed the increase in BP and altered the gut microbiota composition, although it did not significantly change the SCFAs concentration in the cecal contents.

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

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.

Role of alginate in the mechanism by which brown seaweed Saccharina japonica intake alleviates an increase in blood pressure in 2-kidney, 1-clip renovascular hypertensive rats.

BACKGROUND: The intake of Saccharina japonica (SJ), a widely consumed brown seaweed, has been reported to decrease blood pressure (BP) in hypertensive rats. It has been suggested that this effect is related to an increase in fecal sodium excretion (SE) by alginate (Alg) to the gastrointestinal tract; however, the mechanism is still unclear. This study investigated how different seaweeds with different amounts of Alg suppressed BP increase and enhanced fecal SE in 2-kidney, 1-clip renovascular hypertensive (2K1C) rats given SJ diet. METHODS: Rats with 2K1C or sham operation were fed a normal-/high-salt diet with some kinds of seaweeds (5.0%, w/w) or SJ extract with different Alg contents for 6 weeks. We measured systolic BP every week and mean arterial pressure at the end, and measured the total and molecular weights of Alg in each seaweed. Then, we evaluated the relationship of the Alg amount in each seaweed with the suppression of BP increase in 2K1C rats. Finally, urinary and fecal SE for 24 h was measured. RESULTS: The intake of SJ, SJ extract, Saccharina ochotensis (SO) blades and SO roots suppressed BP increase in 2K1C rats, but the strength was not proportional to the amounts of Alg contained in the seaweeds. Although SJ intake increased fecal SE in 2K1C rats fed a high-salt diet, the fecal SE was much less than urinary SE. CONCLUSION: The sodium excretion in feces by Alg in SJ may not be one of the major mechanisms by which SJ intake attenuates hypertension in 2K1C rats.

Dietary capsaicin-mediated attenuation of hypertension in a rat model of renovascular hypertension.

Background: Capsaicin, a pungent component of chili pepper, has been reported to decrease blood pressure (BP) and to cause vasorelaxation via nitric oxide (NO) production. However, it is still unclear how dietary capsaicin effects on renovascular hypertension. To examine this, we observed the effects of dietary capsaicin on BP in 2-kidney, 1-clip renovascular hypertension (2K1C) rats, and investigated the participation of NO in the mechanism.Methods: Rats with 2K1C or sham-operated rats (SHAM) were treated with 0.006% capsaicin diet (CAP) or control diet (CTL) for 6 weeks. Systolic BP (SBP) was measured by tail-cuff method once a week. In the end, mean arterial BP (MAP) was measured in the rats under anesthesia. These observations were performed also in the rats taking a NO synthase (NOS) inhibitor (LN). After rats were euthanized, thoracic aortas were collected and used for western blot analyses to evaluate the phosphorylated ratio of endothelial NOS (eNOS), protein kinase A (PKA) and B (Akt), in order to explore a mechanism of the effects on BP by dietary capsaicin.Results: SBP and MAP in 2K1C rats were significantly higher than in SHAM rats when fed CTL, but not when fed CAP. Those in 2K1C-CAP rats were significantly lower than in 2K1C-CTL rats. LN suppressed the effect of dietary capsaicin. The ratios of phosphorylated (p-) eNOS/eNOS and p-Akt/Akt, but not p-PKA/PKA, were significantly increased in rats fed CAP compared with rats fed CTL.Conclusion: Dietary capsaicin may alleviate 2K1C renovascular hypertension, probably via enhancing phosphorylation of Akt and eNOS.Abbreviations: 2K1C: 2-kidney, 1-clip hypertension model; Akt: protein kinase B; Ang II: angiotensin II; ANOVA: measures analysis of variance; BP: blood pressure; EC: endothelial cell; eNOS: endothelial nitric oxide synthase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; L-NAME, LN: Nω-Nitro-L-arginine methyl ester hydrochloride; MA: mesenteric arteries; MAP: mean arterial blood pressure; NO: nitric oxide; PKA: protein kinase A; PVDF: polyvinylidene difluoride; SBP: Systolic blood pressure; SHR: spontaneously hypertensive rats; SN: sympathetic nervous; TRPV1: transient receptor potential vanilloid type 1; WKY: Wistar Kyoto rats.

Relationship between Self-Rated Health and Lifestyle and Food Habits in Japanese High School Students.

Self-rated health (SRH), a subjective assessment of health status, is extensively used in the field of public health. It is an important and valid measure that is strongly related to morbidity, mortality, longevity and health status. Adolescence is a crucial period for the formation of health status, because health-risk behaviours (e.g., skipping breakfast) are often established during this period. In this study, we investigated the relationship of SRH with lifestyle and eating habits in Japanese high school students. In this study, 1296 students aged 16-18 years from 11 high schools in Japan participated. A questionnaire was administered to these participants that included a question on SRH, five questions on demographic characteristics, six questions on lifestyle items (e.g., wake-up time), five questions on miscellaneous health issues (e.g., anorexia), and 25 questions on food habits and attitudes towards food. We examined the differences between self-rated healthy and unhealthy groups using logistic regression analysis adjusted for gender and age. A dichotomy regression analysis was performed using a stepwise elimination method. Of the 1296 respondents, 16.7% reported feeling unhealthy, 57.7% of whom were females. The self-rated healthy group had a higher frequency of eating breakfast (odds ratio (OR): 2.13; confidence interval (CI): 1.07-4.24) and liked home meals to a greater extent (OR: 3.12; CI: 1.27-7.65) than the self-rated unhealthy group. The two groups did not differ significantly in terms of other lifestyle factors or unidentified complaints. Our results suggest that liking home meals during adolescence may lead to the development of good eating habits, i.e., eating breakfast, and better SRH.

Formulas providing adequate pantothenic acid, vitamin D, manganese, iron and vitamin A for infants fed with mother's milk (aged 6-11 months) according to the Japanese Dietary Reference Intakes prepared by the Ministry of Health, Labour and Welfare (2005 edition).

Weaning formulas served in hospitals and care facilities in Japan should conform to dietary reference intakes (DRIs). We examined whether the DRI for breastfed infants aged 6-11 months can be satisfied in dietary practice, with a particular focus on the fulfilment rates for vitamins, minerals, trace elements and electrolytes in weaning formulas containing energy and protein at levels either greater than or equal to the DRIs, as well as on the dietary profiles of weaning formulas to achieve the DRI for every nutrient. The results showed that no weaning formulas examined in this study fulfilled the DRI for pantothenic acid (5 mg), vitamin D (4 microg), manganese (1.2 mg) or iron (5.5 mg). Furthermore, their vitamin A content exceeded the DRI (350 microg RE). The discrepancy between the guidelines and actual dietary practice is probably because of the fact that the estimated reference values poorly reflect the actual dietary intake in the target population; for example, the pantothenic acid and manganese DRIs for breastfed infants aged 6-11 months were set based on the breast milk intake of younger infants (0-5 months) in combination with the breast milk contents. Our results suggest that dietary guidance for infants should include information to promote proper intakes of vitamins A and D, and iron by reducing the amount of vitamin A-rich foods and utilizing dietary vitamin D and iron supplements including government-approved specified health foods.

Silicosis and smoking strongly increase lung cancer risk in silica-exposed workers.

It remains controversial whether silica is a human lung carcinogen. In this study, we estimated the relative risks of lung cancer due to silica and silicosis by meta-analysis. We collected papers published from 1966-2001 which epidemiologically reported on the relationship between silica/silicosis and lung cancer. We removed papers which did not exclude the effects of asbestos and radioactive materials including radon. We selected the most recent one if some papers were based on the same cohort. Based on the selected papers, we summarized the lung cancer risks from silica, silicosis and non-silicosis with exposure to silica, by meta-analysis using a random effects model. The pooled relative risks were 1.32 (95% confidence interval (CI), 1.23-1.41) for silica, 2.37 (95% CI, 1.98-2.84) for silicosis and 0.96 (95% CI, 0.81-1.15) for non-silicosis with exposure to silica. Since some papers on silica did not exclude silicosis, the risk due to silica itself may be smaller than 1.32. It was less possible that silica exposure directly increases lung cancer risk. On the other hand, the relative risk, 2.37 for silicosis suggested that silicosis increases lung cancer risk. Meta-analysis also revealed that cigarette smoking strongly increased the lung cancer risk in silicotic patients (relative risk, 4.47; 95% CI, 3.17-6.30). Thus, the present study suggested the great importance of preventing silicosis and smoking cessation in reducing lung cancer incidence in silica-exposed workers.

Dietary Zn deficiency does not influence systemic blood pressure and vascular nitric oxide signaling in normotensive rats.

Because zinc (Zn) is an important component for cell protection against certain oxygen species, it has been suggested that Zn deficiency impairs the potent oxidant defense capacity, which is constitutively provided in the vascular system. However, the influence of dietary Zn deficiency on systemic blood pressure and vascular system is controversial and unclear. We therefore examine the effect of dietary Zn deficiency on systemic blood pressure, a potent superoxide scavenger, aortic Cu/Zn superoxide dismutase (SOD) activity, a most representative synthase of the endothelium-derived relaxing factor, and aortic endothelial nitric oxide synthase (eNOS) expression. Furthermore, the direct effects of intravenous administration of NOS inhibitor, Nomega-nitro-L-arginine methyl ester (LNAME), and a SOD mimetic compound, tempol, in normotensives were tested in Wistar-Kyoto (WKY) rats. A Zn-deficient diet (4 wk) contributed to growth retardation, the decrease in thymus weight, and the lower levels of serum Zn compared with the standard diet group. However, no significant difference in conscious systolic and diastolic blood pressure was found in the Zn-deficiency group. The administration of L-NAME caused an increase in the mean arterial pressure (MAP) levels in the two groups of rats and the involvement of the vasodilator nitric oxide (NO) in the regulation of systemic BP in the normotensive state. On the other hand, administration of the superoxide scavenger, tempol, led to a decrease in MAP levels in the two groups of rats, indicating the participation of the oxygen free radical, superoxide, in the maintenance of the systemic BP in a normotensive state. There were no significant differences between the Zn-deficient diet group and the standard diet group in the normotensive state. eNOS expression and Cu/Zn SOD activity in the aorta were also intact in Zn-deficient normotensive rats. These findings suggest that the 4 wk of Zn deficiency was inadequate to alter systemic blood pressure and focal NO signaling in the normotensive state. Long-term Zn deficiency affects the neuronal, immune, and hematopoietic systems, which contribute to systemic and/or local circulation. However, Zn deficiency alone does not cause hypertension and local vascular dysfunction in the normotensive state.

Increased renal vascular resistance in zinc-deficient rats: role of nitric oxide and superoxide.

1. Zinc deficiency (ZD) induces many kinds of pathological states. However, the effects of ZD on haemodynamics remain unclear. In the present study, we measured mean blood pressure (BP) and renal blood flow (RBF) under anaesthesia and calculated renal vascular resistance (RVR) from these parameters in rats maintained on a ZD diet (0.5 p.p.m. zinc) for 4 weeks. 2. Zinc deficiency did not change mean BP, but significantly reduced RBF and increased RVR (each P < 0.01). In addition, these effects of ZD were reversible. 3. Because Cu/Zn superoxide dismutase (SOD) is a zinc-containing enzyme and superoxide is a potent scavenger of nitric oxide (NO), a vasodilator, we hypothesized that one of the mechanisms by which ZD increases RVR is by decreasing NO bioavailability by the enhanced formation of superoxide due to low Cu/Zn SOD activity. To test this hypothesis, we observed the roles of NO and superoxide in the mechanism, after having confirmed the low activity of Cu/Zn SOD in the kidneys of ZD rats. 4. Administration of the SOD mimetic tempol (5 mg/kg per min) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that superoxide was responsible for the mechanism. Low doses of the NO donor sodium nitroprusside (SNP; 2.0 micro g/kg per min, continuous) decreased RVR to a significantly smaller extent in ZD rats compared with control, whereas a high dose of SNP (0.75 mg/kg, bolus) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that the mechanism includes an inhibition of NO activity in ZD, which is most likely to be a scavenging of NO by the activated superoxide. 5. In summary, ZD may increase RVR. The mechanism probably includes changes in NO and superoxide activities.