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

2016 ◽  
Vol 17 (7) ◽  
pp. 1176 ◽  
Author(s):  
Nisha Panth ◽  
Sin-Hee Park ◽  
Hyun Kim ◽  
Deuk-Hoi Kim ◽  
Min-Ho Oak
Keyword(s):  
Protective Effect ◽  
Salt Intake ◽  
Vascular Dysfunction ◽  
High Salt ◽  
Salicornia Europaea ◽  
High Salt Intake

scholarly journals Uncoupling Protein 2 Ablation Exacerbates High-Salt Intake-Induced Vascular Dysfunction

2010 ◽  
Vol 23 (8) ◽  
pp. 822-828 ◽  
Author(s):  
S. Ma ◽  
L. Ma ◽  
D. Yang ◽  
Z. Luo ◽  
X. Hao ◽  
...  
Keyword(s):  
Salt Intake ◽  
Vascular Dysfunction ◽  
Uncoupling Protein ◽  
High Salt ◽  
Uncoupling Protein 2 ◽  
High Salt Intake

Abstract 102: Loss of Salt Sensing Kinase, SGK1, in T Cells Abrogates Memory T Cell Formation, Hypertension, and End-organ Damage

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Hana A Itani ◽  
Arvind Pandey ◽  
Allison E Norlander ◽  
Meenakshi S Madhur ◽  
David G Harrison
Keyword(s):  
T Cells ◽  
T Cell ◽  
Salt Intake ◽  
Memory T Cells ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Cell Formation ◽  
Salt Sensitivity ◽  
High Salt ◽  
High Salt Intake

Accumulating evidence indicates that NaCl can be concentrated in tissues with high salt-intake, age and in the setting of hypertension. Elevated NaCl has been shown to promote T H 17 cell formation in an SGK1-dependent fashion. We have previously shown that Memory T cells play a major role in the genesis of hypertension. These long-lived cells remain responsive to repeated hypertensive stimuli, such as salt feeding, and can be mobilized to enter the kidney where they release cytokines that promote renal dysfunction. To examine mechanisms by which T cells sense salt and contribute to salt-sensitivity, we tested the hypothesis that SGK1 in T cells is necessary for formation of memory T cells and their activation in salt-sensitive hypertension. To study the role of SKG1 in hypertension, we produced mice with T cell specific deletion of SGK1, SGK1 fl/fl x tg CD4cre mice and used SGK1 fl/fl mice as controls. To impose repeated episodes of hypertension, we treated these mice with L-NAME (0.5mg/ml) in drinking water for two weeks, allowed a two-week normotensive interval and a then fed high salt (4% NaCl) for three weeks. L-NAME followed by high salt increased memory T cells in the kidney, aorta and bone marrow of SGK1 fl/fl control mice but not in SGK1 fl/fl x tg CD4cre mice, as identified by the surface marker CD44 hi . To assess markers of renal injury, we measured albumin in 24-hour urine samples collected at the end of the L-NAME/high salt. L-NAME/high salt caused striking albuminuria in SGK1 fl/fl mice and was absent in SGK1 fl/fl x tg CD4cre mice. In additional studies, we found that loss of SGK1 in T cells abrogates renal and vascular inflammation and protects against hypertensive renal and vascular injury in the L-NAME/high salt model. Thus, our data provide a potential mechanism by which SGK1 in T cells promotes their development of salt sensitivity and their mediation of renal and vascular dysfunction in hypertension.

scholarly journals Protective Effect of Gamma Aminobutyric Acid against Aggravation of Renal Injury Caused by High Salt Intake in Cisplatin-Induced Nephrotoxicity

2022 ◽  
Vol 23 (1) ◽  
pp. 502
Author(s):  
Hyesook Lee ◽  
Seon Yeong Ji ◽  
Hyun Hwangbo ◽  
Min Yeong Kim ◽  
Da Hye Kim ◽  
...  
Keyword(s):  
Protective Effect ◽  
Renal Injury ◽  
Salt Intake ◽  
Protective Efficacy ◽  
High Salt ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Renal Hypertrophy ◽  
High Salt Intake

Gamma-aminobutyric acid (GABA) is one of the inhibitory neurotransmitters. Several studies have suggested that GABA supplements can reduce blood pressure and modulate the renal immune system in vitro and in vivo. In the present study, we investigated the effect of GABA-enriched salt as an alternative to traditional salt on aggravated renal injury by high salt intake in cisplatin-induced nephrotoxicity mice. High salt intake accelerated the increase of biomarkers, such as blood urea nitrogen and serum creatinine levels for renal injury in cisplatin-induced nephrotoxicity mice. However, oral administration of GABA-contained salt notably suppressed serum BUN and creatinine levels. The efficacy of GABA salt was superior to lacto GABA salt and postbiotics GABA salt. Furthermore, GABA-enriched salt markedly restored histological symptoms of nephrotoxicity including renal hypertrophy, tubular dilation, hemorrhage, and collagen deposition aggravated by salt over-loading in cisplatin-exposed mice. Among them, GABA salt showed a higher protective effect against cisplatin-induced renal histological changes than lacto GABA salt and postbiotics GABA salt. In addition, administration of high salt significantly enhanced expression levels of apoptosis and inflammatory mediators in cisplatin-induced nephrotoxicity mice, while GABA-enriched salt greatly down-regulated the expression of these mediators. Taken together, these results demonstrate the protective effect of GABA against damage caused by high salt intake in cisplatin-induced renal toxicity. Its mechanism may be due to the suppression of hematological and biochemical toxicity, apoptosis, and inflammation. In conclusion, although the protective efficacy of GABA salt on renal injury is different depending on the sterilization and filtration process after fermentation with L. brevis BJ20 and L. plantarum BJ21, our findings suggest that GABA-enriched salt has a beneficial effect against immoderate high salt intake-mediated kidney injury in patients with cisplatin-induced nephrotoxicity.

scholarly journals High Salt Intake and Stroke: Meta-analysis of the Epidemiologic Evidence

2012 ◽  
Vol 18 (8) ◽  
pp. 691-701 ◽  
Author(s):  
Xiu-Yang Li ◽  
Xian-Lei Cai ◽  
Ping-Da Bian ◽  
Liu-Ru Hu
Keyword(s):  
Salt Intake ◽  
Meta Analysis ◽  
High Salt ◽  
Epidemiologic Evidence ◽  
High Salt Intake

scholarly journals Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

2011 ◽  
Vol 209 (1) ◽  
pp. 85-94 ◽  
Author(s):  
Karine Bibeau ◽  
Mélissa Otis ◽  
Jean St-Louis ◽  
Nicole Gallo-Payet ◽  
Michèle Brochu
Keyword(s):  
Protein Expression ◽  
Adrenal Glands ◽  
Salt Intake ◽  
High Salt ◽  
Receptor Subtypes ◽  
Mrna Levels ◽  
Female Rat ◽  
Angiotensin Ii Receptor ◽  
Intrauterine Growth ◽  
High Salt Intake

In low sodium-induced intrauterine growth restricted (IUGR) rat, foetal adrenal steroidogenesis as well as the adult renin–angiotensin–aldosterone system (RAAS) is altered. The aim of the present study was to determine the expression of cytochrome P450 aldosterone synthase (P450aldo) and of angiotensin II receptor subtypes 1 (AT1R) and 2 (AT2R) in adult adrenal glands and whether this expression could be influenced by IUGR and by high-salt intake in a sex-specific manner. After 6 weeks of 0.9% NaCl supplementation, plasma renin activity, P450aldo expression and serum aldosterone levels were decreased in all groups. In males, IUGR induced an increase in AT1R, AT2R, and P450aldo levels, without changes in morphological appearance of the zona glomerulosa (ZG). By contrast, in females, IUGR had no effect on the expression of AT1R, but increased AT2R mRNA while decreasing protein expression of AT2R and P450aldo. In males, salt intake in IUGR rats reduced both AT1R mRNA and protein, while for AT2R, mRNA levels decreased whereas protein expression increased. In females, salt intake reduced ZG size in IUGR but had no affect on AT1R or AT2R expression in either group. These results indicate that, in response to IUGR and subsequently to salt intake, P450aldo, AT1R, and AT2R levels are differentially expressed in males and females. However, despite these adrenal changes, adult IUGR rats display adequate physiological and adrenal responses to high-salt intake, via RAAS inhibition, thus suggesting that extra-adrenal factors likely compensate for ZG alterations induced by IUGR.

scholarly journals High fat and/or high salt intake during pregnancy alters maternal meta-inflammation and offspring growth and metabolic profiles

2014 ◽  
Vol 2 (8) ◽  
pp. e12110 ◽  
Author(s):  
Clare M. Reynolds ◽  
Mark H. Vickers ◽  
Claudia J. Harrison ◽  
Stephanie A. Segovia ◽  
Clint Gray
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Metabolic Profiles ◽  
High Fat ◽  
High Salt Intake ◽  
Offspring Growth
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