scholarly journals Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

2000 ◽  
pp. 524-532 ◽  
Author(s):  
S Deloof ◽  
C De Seze ◽  
V Montel ◽  
A Chatelain
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Adrenal Glands ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
Fetal Rats

OBJECTIVE: This study aimed at determining, in the term pregnant rat, whether maternal and fetal plasma atrial natriuretic peptide (ANP) concentrations were modified in response to an oral sodium load, and to investigate whether any changes in plasma concentrations were able to modify the density and affinity of the different ANP-binding site subtypes in maternal and fetal kidneys and adrenal glands. METHODS: Pregnant rats kept in metabolic cages were divided into two groups. The normal sodium diet group had free access to rat chow and tap water whereas the high sodium diet group received 1% NaCl as drinking water for 10 consecutive days from day 11 to day 21 of gestation with free access to standard rat chow. Pregnant rats from both groups were killed by decapitation on day 21 of gestation. The plasma ANP and aldosterone concentrations were determined by RIA. The density and affinity of ANP receptors were determined in the maternal and fetal adrenal glands and kidneys. RESULTS: In the pregnant rats on the high-salt diet, the sodium and water intakes, as well as the urine volume and sodium excretion, were significantly higher than in the control group. After 10 days of high-salt intake, water and sodium retentions were not significantly different in the two groups, indicating that the pregnant rats were able to excrete excess salt. The high sodium intake did not change the body weight of the pregnant rats but did increase the body weight of the fetal rats. Maternal and fetal hematocrits remained unchanged in both groups, the high sodium intake did not modify plasma sodium concentration in the maternal rats but increased that of the fetuses, indicating an accumulation of sodium in the fetal rats. The dietary sodium intake did not change the plasma ANP concentrations but significantly decreased the plasma aldosterone concentrations in both the maternal and fetal rats. In response to the high-salt diet, the density and affinity of total ANP, ANPb and ANPc receptors were not altered in the maternal isolated renal glomeruli or the adrenal zona glomerulosa membranes or the fetal adrenal gland and kidney membrane preparations. CONCLUSION: These results suggest that ANP is not involved in the regulation of water and electrolyte balance in maternal and fetal rats during salt-loaded intake.

scholarly journals Renal Overexpression of Atrial Natriuretic Peptide and Hypoxia Inducible Factor-1αas Adaptive Response to a High Salt Diet

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Silvana Lorena Della Penna ◽  
Gabriel Cao ◽  
Andrea Carranza ◽  
Elsa Zotta ◽  
Susana Gorzalczany ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Adaptive Response ◽  
Hypoxia Inducible Factor ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sodium Overload ◽  
Atrial Natriuretic

In the kidney, a high salt intake favors oxidative stress and hypoxia and causes the development of fibrosis. Both atrial natriuretic peptide (ANP) and hypoxia inducible factor (HIF-1α) exert cytoprotective effects. We tested the hypothesis that renal expression of ANP and HIF-1αis involved in a mechanism responding to the oxidative stress produced in the kidneys of rats chronically fed a high sodium diet. Sprague-Dawley rats were fed with a normal salt (0.4% NaCl) (NS) or a high salt (8% NaCl) (HS) diet for 3 weeks, with or without the administration of tempol (T), an inhibitor of oxidative stress, in the drinking water. We measured the mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (UVNa). We evaluated the expression of ANP, HIF-1α, and transforming growth factor (TGF-β1) in renal tissues by western blot and immunohistochemistry. The animals fed a high salt diet showed increased MAP andUVNalevels and enhanced renal immunostaining of ANP, HIF-1α, and TGF-β1. The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-β1, and HIF-1αcompared to their control. These findings suggest that HIF-1αand ANP, synthesized by the kidney, are involved in an adaptive mechanism in response to a sodium overload to prevent or attenuate the deleterious effects of the oxidative stress and the hypoxia on the development of fibrosis.Erratum to “Renal Overexpression of Atrial Natriuretic Peptide and Hypoxia Inducible Factor-1α as Adaptive Response to a High Salt Diet”

Effect of saline infusion on kidney and collecting duct function in atrial natriuretic peptide (ANP) gene "knockout" mice

1999 ◽  
Vol 77 (6) ◽  
pp. 454-457 ◽  
Author(s):  
U Honrath ◽  
C K Chong ◽  
L G Melo ◽  
Harald Sonnenberg
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Collecting Duct ◽  
High Salt ◽  
Saline Infusion ◽  
Kidney Weight ◽  
High Salt Diet ◽  
Salt Diet ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is thought to play a role in renal regulation of salt balance by reducing tubular reabsorption of sodium and chloride. Therefore, in the chronic absence of this hormone, a defect of salt excretion should be evident. We used an ANP gene deletion model to test this premise. F2 homozygous mutant mice (-/-) and their wild-type littermates (+/+) were fed an 8% NaCl diet prior to an acute infusion of isotonic saline. Arterial blood pressures, renal excretions of salt and water, as well as collecting duct transport of fluid and electrolytes were measured. Pressures were significantly higher in -/- compared with +/+ mice (139 ± 4 vs. 101 ± 2 mmHg; 1 mmHg = 133.3 Pa). There was no difference in glomerular filtration rate (-/- = 0.84 ± 0.06; +/+ = 0.81 ± 0.04 mL·min-1·g-1 kidney weight). In the collecting duct, sodium and chloride reabsorptions were significantly higher in the -/- group than in the +/+ group. As a result, natriuresis and chloruresis were relatively reduced (UNaV: -/- = 8.6 ± 1.1; +/+ = 14.0 ± 1.1; UClV: -/- = 10.1 ± 1.4; +/+ = 16.0 ± 1.1 µmol·min-1·g-1 kidney weight). We conclude that the absence of endogenous ANP activity in mice on a high-salt diet subjected to acute saline infusion causes inappropriately high reabsorption of sodium and chloride in the medullary collecting duct, resulting in a relative defect in renal excretory capacity for salt.Key words: high-salt diet; water, sodium, chloride, and potassium transport.

Renal endothelin in chronic angiotensin II hypertension

2002 ◽  
Vol 283 (1) ◽  
pp. R243-R248 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Jennifer S. Pollock ◽  
David M. Pollock
Keyword(s):  
Sodium Intake ◽  
Renal Tissue ◽  
High Salt ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Outer Medulla ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Saline Vehicle

To determine the influence of chronic ANG II infusion on urinary, plasma, and renal tissue levels of immunoreactive endothelin (ET), ANG II (65 ng/min) or saline vehicle was delivered via osmotic minipump in male Sprague-Dawley rats given either a high-salt diet (10% NaCl) or normal-salt diet (0.8% NaCl). High-salt diet alone caused a slight but not statistically significant increase (7 ± 1%) in mean arterial pressure (MAP). MAP was significantly increased in ANG II-infused rats (41 ± 10%), and the increase in MAP was significantly greater in ANG II rats given a high-salt diet (59 ± 1%) compared with the increase observed in rats given a high-salt diet alone or ANG II infusion and normal-salt diet. After a 2-wk treatment, urinary excretion of immunoreactive ET was significantly increased by ∼50% in ANG II-infused animals and by over 250% in rats on high-salt diet, with or without ANG II infusion. ANG II infusion combined with high-salt diet significantly increased immunoreactive ET content in the cortex and outer medulla, but this effect was not observed in other groups. In contrast, high-salt diet, with or without ANG II infusion, significantly decreased immunoreactive ET content within the inner medulla. These data indicate that chronic elevations in ANG II levels and sodium intake differentially affect ET levels within the kidney and provide further support for the hypothesis that the hypertensive effects of ANG II may be due to interaction with the renal ET system.

Salt intake and insulin sensitivity in healthy human volunteers

2007 ◽  
Vol 113 (3) ◽  
pp. 141-148 ◽  
Author(s):  
Raymond R. Townsend ◽  
Shiv Kapoor ◽  
Christopher B. McFadden
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Infusion ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Euglycaemic Clamp ◽  
Noradrenaline Concentration ◽  
Low Salt

The literature on salt intake and insulin sensitivity presents a mixed picture, as some studies have shown an increase, whereas others have shown a decrease, in insulin action as sodium intake is enhanced. In some cases, this may relate to the study of salt intake in patients with co-morbidities such as hypertension or diabetes. In the present study, we selected healthy normotensive lean volunteers who underwent a euglycaemic clamp following 6 days of a low-salt diet (20 mmol sodium daily) and, subsequently, 6 days of a high-salt diet (200 mmol sodium daily). Our results show an increase in insulin-mediated glucose disposal during euglycaemic clamp conditions that was significantly higher following the high-salt diet compared with the low-salt diet (7.41±0.41 compared with 6.11±0.40 mg·kg−1 of body weight·min−1 respectively; P=0.03). We measured calf blood flow before and during insulin infusion (no significant change after the two dietary salt interventions was detected) and plasma non-esterified fatty acids (also no significant differences were detected). We observed the expected increases in renin concentration and aldosterone activity in subjects on the low-salt diet, and also observed a significantly less increase in plasma noradrenaline concentration during euglycaemic insulin infusion following the high-salt compared with the low-salt diet. We propose that the 4–5-fold increase in serum aldosterone and the greater increase in plasma noradrenaline concentration following the low-salt intervention compared with the high-salt period may have contributed to the differences in insulin sensitivity following the adjustment in dietary sodium intake.

scholarly journals Studies of Salt and Stress Sensitivity on Arterial Pressure in Renin-b Deficient Mice

2021 ◽  
Author(s):  
Pablo Nakagawa ◽  
Javier Gomez ◽  
Ko-Ting Lu ◽  
Justin L. Grobe ◽  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Sodium Intake ◽  
High Salt ◽  
Ventrolateral Medulla ◽  
High Salt Diet ◽  
Blood Pressure Elevation ◽  
Salt Diet ◽  
The Brain ◽  
Deficient Mice

AbstractExcessive sodium intake is known to increase the risk for hypertension, heart disease, and stroke. Individuals who are more susceptible to the effects of high salt are at higher risk for cardiovascular diseases even independent of their blood pressure status. Local activation of the renin-angiotensin system (RAS) in the brain, among other mechanisms, has been hypothesized to play a key role in contributing to salt balance. We have previously shown that deletion of the alternative renin isoform termed renin-b disinhibits the classical renin-a encoding preprorenin in the brain resulting in elevated brain RAS activity. Thus, we hypothesized that renin-b deficiency results in higher susceptibility to salt-induced elevation in blood pressure. Telemetry implanted Ren-bNull and wildtype littermate mice were first offered a low salt diet for a week and subsequently a high salt diet for another week. A high salt diet induced a mild blood pressure elevation in both Ren-bNull and wildtype mice, but mice lacking renin-b did not exhibit an exaggerated pressor response. When renin-b deficient mice were exposed to a high salt diet for a longer duration (4 weeks), was a trend for increased myocardial enlargement in Ren-bNull mice when compared with control mice. Multiple studies have also demonstrated the association of chronic and acute environmental stress with hypertension. Activation of the RAS in the rostral ventrolateral medulla and the hypothalamus is required for stress-induced hypertension. Thus, we next questioned whether the lack of renin-b would result in exacerbated response to an acute restraint-stress. Wildtype and Ren-bNull mice equally exhibited elevated blood pressure in response to restraint-stress, which was similar in mice fed either a low or high salt diet. These studies highlight a complex mechanism that masks/unmasks roles for renin-b in cardiovascular physiology.

scholarly journals Effects of water deprivation on atrial natriuretic peptide secretion and density of binding sites in adrenal glands and kidneys of maternal and fetal rats in late gestation

1999 ◽  
pp. 160-168 ◽  
Author(s):  
S Deloof ◽  
C De Seze ◽  
V Montel ◽  
A Chatelain
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Water Deprivation ◽  
Adrenal Glands ◽  
Zona Glomerulosa ◽  
Receptor Density ◽  
Renal Glomeruli ◽  
Fetal Rats ◽  
Anp Receptors ◽  
Atrial Natriuretic

The effects of water deprivation for 3 days were studied in pregnant rats and their fetuses on day 21 of gestation. Maternal water deprivation induced a significant decrease of the body weight in both maternal and fetal rats. This weight loss was accompanied by significant increases in plasma osmolality and haematocrit in both maternal and fetal rats. Similarly, dehydration significantly decreased plasma atrial natriuretic peptide (ANP) concentrations and increased plasma aldosterone concentrations in maternal and fetal rats. Water-deprived maternal rats presented a significant increase in total ANP receptor density in isolated renal glomeruli and adrenal zona glomerulosa membranes. This increase was due to a significant increase in ANPc receptor density in both renal glomeruli and adrenal zona glomerulosa. The densities of total ANP, ANPb and ANPc receptors in fetal kidneys and adrenal glands were not affected by maternal dehydration. These results suggest that the dehydrated maternal rat is able to up-regulate the number of its ANP receptors in its kidneys and adrenal glands, in response to a decrease in plasma ANP concentrations. In contrast, the fetal rat does not seem to be able to regulate its own ANP receptors in response to maternal dehydration, in spite of a decrease in plasma ANP concentrations.

scholarly journals High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 883
Author(s):  
Ghassan Bkaily ◽  
Yanick Simon ◽  
Ashley Jazzar ◽  
Houssein Najibeddine ◽  
Alexandre Normand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
High Salt ◽  
Vascular Endothelial ◽  
High Cardiovascular Risk ◽  
High Salt Diet ◽  
Salt Diet ◽  
Lower Survival Rate ◽  
High Sodium ◽  
Induced Hypertension

Our knowledge on essential hypertension is vast, and its treatment is well known. Not all hypertensives are salt-sensitive. The available evidence suggests that even normotensive individuals are at high cardiovascular risk and lower survival rate, as blood pressure eventually rises later in life with a high salt diet. In addition, little is known about high sodium (Na+) salt diet-sensitive hypertension. There is no doubt that direct and indirect Na+ transporters, such as the Na/Ca exchanger and the Na/H exchanger, and the Na/K pump could be implicated in the development of high salt-induced hypertension in humans. These mechanisms could be involved following the destruction of the cell membrane glycocalyx and changes in vascular endothelial and smooth muscle cells membranes’ permeability and osmolarity. Thus, it is vital to determine the membrane and intracellular mechanisms implicated in this type of hypertension and its treatment.

Abstract P280: Novel Insights into Transcriptional Regulation of the Human Angiotensinogen Gene by High-salt: A Study in Transgenic Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Meenakshi Kaw ◽  
Sudhir Jain ◽  
Shravan Perla Perla ◽  
Natalie Sirianni ◽  
Mariam Alakrawi Alakrawi ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Lifestyle Changes ◽  
High Salt ◽  
Risk Haplotype ◽  
Chip Assay ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

Angiotensinogen is the substrate for the entire RAS cascade and polymorphisms leading to its overexpression are linked to hypertension. SNPs in the promoter of the hAGT gene are associated with hypertension. Importantly, these SNPs can further modulate the gene of interest in various physiological/environmental settings like the high-sodium diet. In this regard, the human angiotensinogen (hAGT) gene has polymorphisms in its 2.5Kb promoter that form two haplotype (Hap) blocks: -6A/G (-1670A/G, -1562C/T, -1561T/C) and -217A/G (-532T/C, -793A/G, -1074T/C, and -1178G/A). Hap -6A/-217A is associated with human hypertension whereas Hap -6G/-217G reduces cardiovascular risk. We have engineered transgenic (TG) mice with these haplotypes (Hap -6A: -6A/-217A and Hap -6G: -6G/-217G) so as to examine the transcriptional regulation of the hAGT in an in vivo setting. This study is designed to study the effects of a high-sodium diet on the transcriptional milieu of renal tissues with consequential effects on the hAGT expression in our two haplotypes. Male TG mice were placed on 4% Na + diet for a period of 8 weeks. High-salt diet induces mineralocorticoid receptor (MR) and SGK-kinase expression in both haplotypes, equally. MR has been shown to bind to GRE elements in the hAGT gene. Importantly, MR-binding (ChIP assay) and hAGT induction are significantly (p<0.05) greater in the -6A haplotype males as compared to -6G males. High-salt also increased the expression of transcriptional regulators including CEBPβ and HNF4 (p<0.05) that are independent of haplotype. Complementary ChIP assay confirmed enhanced transcription factor (TF) binding to the chromatin of male -6A TG mice as compared to their -6G counterparts after high-salt diet treatment. Thus, we show here an effect of high-salt on cellular transcriptional apparatus that is haplotype-independent. However, increased TF affinity of the chromatin in -6A TG mice leads to higher salt-induced AGT levels in this haplotype than -6G. These observations could partly account for increased salt-sensitivity of some adult males that, in turn, is governed by the “risk” haplotype. Identifying these individuals with the -6A haplotype will help guide therapeutic lifestyle changes in patients with essential hypertension.

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