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  1. Campbell NRC, Whelton PK, Orias M, Wainford RD, Cappuccio FP, Ide N, et al.
    J Hum Hypertens, 2023 Jun;37(6):428-437.
    PMID: 35581323 DOI: 10.1038/s41371-022-00690-0
    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects
  2. Lai JS, Tan CK, Yusoff K, Cheah SC
    Biotechnol Appl Biochem, 2023 Apr;70(2):603-612.
    PMID: 35830743 DOI: 10.1002/bab.2383
    Excessive salt consumption has been associated with greater risk of hypertension. Therefore, monitoring of dietary sodium consumption should be prioritized. As sodium is mainly excreted through urine, 24-h urine sample can be used to estimate individual sodium intake. Thus, a simple and inexpensive semi-quantitative urinary sodium detection test strip was developed based on the enzymatic reaction between β-galactosidase and chlorophenol red-β-d-galactopyranoside. When tested, color formation was distinguished at 0 M (chartreuse yellow), 0.05 M (sunflower), 0.1-0.15 M (mango tango), and 0.2-0.25 M (persimmon) sodium. Analysis from ImageJ showed a linear result (r2  > 0.9), low SD, and significant increase in magenta difference (p sodium. Test strip can detect 0.03 M sodium at minimum but did not last for >2 days in adverse storage conditions (laboratory conditions, ∼80% relative humidity, 40°C, and direct light exposure) when stored in test strip bottles, and even shorter when exposed to the environment. The presence of urinary potassium, urea, and glucose did not affect test strip performance. Test strip produced comparable results to flame photometry with <15% variation when tested on overnight, random spot, and 24-h urine samples. Overall, the developed test strip can be used to enzymatically semi-quantify 0.05-0.25 M sodium.
    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects
  3. Campbell NRC, Whelton PK, Orias M, Cobb LL, Jones ESW, Garg R, et al.
    J Hypertens, 2023 May 01;41(5):683-686.
    PMID: 36723484 DOI: 10.1097/HJH.0000000000003385
    Spot urine samples with estimating equations have been used to assess individuals' sodium (salt) intake in association with health outcomes. There is large random and systematic error in estimating sodium intake using this method and spurious health outcome associations. Substantial controversy has resulted from false claims the method is valid. Hence, the World Hypertension League, International Society of Hypertension and Resolve to Save Lives, supported by 21 other health organizations, have issued this policy statement that strongly recommends that research using spot urine samples with estimating equations to assess individuals' sodium (salt) intake in association with health outcomes should not be conducted, funded or published. Literature reviews on the health impacts of reducing dietary sodium that include studies that have used spot and short duration timed urine samples with estimating equations need to explicitly acknowledge that the method is not recommended to be used and is associated with spurious health outcome associations.
    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects
  4. Muraya N, Kadowaki D, Miyamura S, Kitamura K, Uchimura K, Narita Y, et al.
    Oxid Med Cell Longev, 2018;2018:7635274.
    PMID: 29967665 DOI: 10.1155/2018/7635274
    Oxidative stress induced by hyperuricemia is closely associated with the renin-angiotensin system, as well as the onset and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). It is therefore important to reduce oxidative stress to treat hyperuricemia. We previously found that benzbromarone, a uricosuric agent, has a direct free radical scavenging effect in vitro. The antioxidant effects of benzbromarone were evaluated in vivo via oral administration of benzbromarone for 4 weeks to model rats with angiotensin II- and salt-induced hypertension. Benzbromarone did not alter plasma uric acid levels or blood pressure but significantly reduced the levels of advanced oxidation protein products, which are oxidative stress markers. Furthermore, dihydroethidium staining of the kidney revealed a reduction in oxidative stress after benzbromarone administration. These results suggest that benzbromarone has a direct antioxidant effect in vivo and great potential to prevent CVD and CKD.
    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects
  5. Gupta T, Connors M, Tan JW, Manosroi W, Ahmed N, Ting PY, et al.
    Am J Hypertens, 2017 Dec 08;31(1):124-131.
    PMID: 28985281 DOI: 10.1093/ajh/hpx146
    BACKGROUND: Understanding the interactions between genetics, sodium (Na+) intake, and blood pressure (BP) will help overcome the lack of individual specificity in our current treatment of hypertension. This study had 3 goals: expand on the relationship between striatin gene (STRN) status and salt-sensitivity of BP (SSBP); evaluate the status of Na+ and volume regulating systems by striatin risk allele status; evaluate potential SSBP mechanisms.

    METHODS: We assessed the relationship between STRN status in humans (HyperPATH cohort) and SSBP and on volume regulated systems in humans and a striatin knockout mouse (STRN+/-).

    RESULTS: The previously identified association between a striatin risk allele and systolic SSBP was demonstrated in a new cohort (P = 0.01). The STRN-SSBP association was significant for the combined cohort (P = 0.003; β = +5.35 mm Hg systolic BP/risk allele) and in the following subgroups: normotensives, hypertensives, men, and older subjects. Additionally, we observed a lower epinephrine level in risk allele carriers (P = 0.014) and decreased adrenal medulla phenylethanolamine N-methyltransferase (PNMT) in STRN+/- mice. No significant associations were observed with other volume regulated systems.

    CONCLUSIONS: These results support the association between a variant of striatin and SSBP and extend the findings to normotensive individuals and other subsets. In contrast to most salt-sensitive hypertensives, striatin-associated SSBP is associated with normal plasma renin activity and reduced epinephrine levels. These data provide clues to the underlying cause and a potential pathway to achieve, specific, personalized treatment, and prevention.

    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects*
  6. Ramachandran CD, Gholami K, Lam SK, Hoe SZ
    Exp Biol Med (Maywood), 2023 Oct;248(20):1768-1779.
    PMID: 37828834 DOI: 10.1177/15353702231198085
    An increase in blood pressure by a high-salt (HS) diet may change the expression levels of renal epithelial sodium channels (ENaCs) and aquaporins (AQPs). Spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were exposed to HS and regular-salt (RS) diets for 6 weeks. Mean arterial pressure (MAP) and plasma atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone, and arginine vasopressin (AVP) levels were determined. Expression of mRNA levels of ENaCs and AQPs were quantified by real-time PCR. The MAP was higher in SHRs on the HS diet. Plasma Ang II and aldosterone levels were low while plasma ANP level was high in both strains of rats. Renal expression of mRNA levels of α-, β-, and γ-ENaCs was lowered in SHRs on the HS diet. Meanwhile, renal AQP1, AQP2, and AQP7 mRNA expression levels were lowered in both strains of rats on the HS diet. Suppression of mRNA expression levels of ENaC and AQP subunits suggests that the high-salt-induced increase in the MAP of SHR may not be solely due to renal sodium and water retention.
    Matched MeSH terms: Sodium Chloride, Dietary/adverse effects
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