scholarly journals High Salt Diet Affects the Reproductive Health in Animals: An Overview

Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 590
Author(s):  
Sameh A. Abdelnour ◽  
Mohamed E. Abd El-Hack ◽  
Ahmed E. Noreldin ◽  
Gaber Elsaber Batiha ◽  
Amani Magdy Beshbishy ◽  
...  
Keyword(s):  
Growth Performance ◽  
Cell Function ◽  
Salt Intake ◽  
Ovarian Follicle ◽  
Productivity Loss ◽  
Crop Productivity ◽  
High Salt ◽  
Inflammatory Factors ◽  
Hormone Regulation ◽  
High Salt Intake

Salinity is a reliable issue of crop productivity loss in the world and in certain tropical and subtropical zones. However, tremendous progress in the genetic improvement of plants for salinity tolerance has been made over several decades. In light of this, halophytic plants can be used as animal feeds and have promising features because they are a good feed resource. However, the main constraint of saline pasture systems is the extreme concentration of NaCl salt in drinking water and forage plants for grazing animals. Ecological reports revealed that excess diet salt causes mortality and morbidity worldwide. Animal fed halophytic forages may have adverse effects on growth performance and reproductive function in males and females due to inducing reductions in hormone regulation, such as testosterone, FSH, LH, and leptin. It was indicated that high salt intake promotes circulating inflammatory factors in the placenta and is associated with adversative effects on pregnancy. This review focuses on the scientific evidence related to the effect of high salt intake on growth performance, spermatogenesis, sperm function, and testicular morphology changes in male animals. In addition, the review will also focus on its effect on some female reproductive features (e.g., ovarian follicle developments, placental indices, and granulosa cell function).

High salt intake negatively impacts ovarian follicle development

2015 ◽  
Vol 200 ◽  
pp. 79-87 ◽  
Author(s):  
Guang Wang ◽  
Cheung-Kwan Yeung ◽  
Jing-Li Zhang ◽  
Xi-Wen Hu ◽  
Yu-Xiang Ye ◽  
...  
Keyword(s):  
Salt Intake ◽  
Ovarian Follicle ◽  
High Salt ◽  
Follicle Development ◽  
Ovarian Follicle Development ◽  
High Salt Intake

Effect of salt intake on endothelium-derived factors in a group of patients with essential hypertension

2001 ◽  
Vol 101 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Ernesto BRAGULAT ◽  
Alejandro de la SIERRA ◽  
María T. ANTONIO ◽  
Wladimiro JIMÉNEZ ◽  
Álvaro URBANO-MÁRQUEZ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Concentration ◽  
Urinary Excretion ◽  
Plasma Levels ◽  
Cell Function ◽  
Salt Intake ◽  
High Salt ◽  
Endothelial Cell Function ◽  
High Salt Intake

The aim of the present study was to evaluate the effects of the level of salt intake on endothelium-derived factors in a group of patients with essential hypertension. A group of 50 patients with essential hypertension who had never been treated for the condition were placed on a low-sodium (50 mmol/day), low-nitrate (400 µmol/day) diet, which was supplemented, in a single-blind fashion, with placebo tablets for the first 7 days and then with NaCl tablets (200 mmol/day) for a further 7 days (total sodium intake 250 mmol/day). At the end of both periods, 24-h ambulatory blood pressure monitoring was performed. In addition, plasma levels and 24-h urinary excretion of nitrites plus nitrates and cGMP were measured, along with plasma levels of endothelin. A high salt intake promoted significant decreases in plasma levels of nitrites plus nitrates (from 41.0±2.1 to 32.8±1.8 nmol/ml; P < 0.001), 24-h urinary nitrate excretion (from 417±36 to 334±37 µmol/24 h; P = 0.045) and plasma endothelin levels (from 5.6±0.3 to 4.6±0.3 pg/ml; P = 0.007). The plasma concentration and 24-h urinary excretion of cGMP were not altered significantly by a high salt intake. We did not find any relationship between endothelium-derived products and 24-h mean blood pressure, at either low or high salt intakes, or between changes induced by the high-salt diet. A high salt intake also induced significant decreases in plasma renin activity, angiotensin II and aldosterone, and a significant increase in atrial natriuretic peptide. We conclude that a high salt intake decreases the plasma concentration and urinary excretion of nitrates and plasma levels of endothelin in patients with essential hypertension, suggesting that the level of salt intake may affect endothelial cell function. However, these alterations are not correlated with changes in blood pressure induced by the high salt intake.

Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake

2011 ◽  
Vol 301 (2) ◽  
pp. F263-F270 ◽  
Author(s):  
M. C. Fiore ◽  
P. M. Jimenez ◽  
D. Cremonezzi ◽  
L. I. Juncos ◽  
N. H. García
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Body Weight ◽  
Salt Intake ◽  
High Salt ◽  
Lipid Lowering ◽  
Inflammatory Factors ◽  
Glomerular Volume ◽  
High Salt Intake ◽  
Tgf Β1

High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-β1 expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetylcholine-induced vasodilatation decreased by 40.4% in HS rats ( P < 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-β1. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.

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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