scholarly journals High sodium intake increases HCO3− absorption in medullary thick ascending limb through adaptations in basolateral and apical Na+/H+ exchangers

2011 ◽  
Vol 301 (2) ◽  
pp. F334-F343 ◽  
Author(s):  
David W. Good ◽  
Thampi George ◽  
Bruns A. Watts
Keyword(s):  
Absorptive Capacity ◽  
Sodium Intake ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
High Sodium ◽  
High Sodium Intake ◽  
Medullary Thick Ascending Limb ◽  
Nhe1 Activity ◽  
Exchange Activity

A high sodium intake increases the capacity of the medullary thick ascending limb (MTAL) to absorb HCO3−. Here, we examined the role of the apical NHE3 and basolateral NHE1 Na+/H+ exchangers in this adaptation. MTALs from rats drinking H2O or 0.28 M NaCl for 5–7 days were perfused in vitro. High sodium intake increased HCO3− absorption rate by 60%. The increased HCO3− absorptive capacity was mediated by an increase in apical NHE3 activity. Inhibiting basolateral NHE1 with bath amiloride eliminated 60% of the adaptive increase in HCO3− absorption. Thus the majority of the increase in NHE3 activity was dependent on NHE1. A high sodium intake increased basolateral Na+/H+ exchange activity by 89% in association with an increase in NHE1 expression. High sodium intake increased apical Na+/H+ exchange activity by 30% under conditions in which basolateral Na+/H+ exchange was inhibited but did not change NHE3 abundance. These results suggest that high sodium intake increases HCO3− absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. These studies support a role for NHE1 in the long-term regulation of renal tubule function and suggest that the regulatory interaction whereby NHE1 enhances the activity of NHE3 in the MTAL plays a role in the chronic regulation of HCO3− absorption. The adaptive increases in Na+/H+ exchange activity and HCO3− absorption in the MTAL may play a role in enabling the kidneys to regulate acid-base balance during changes in sodium and volume balance.

Adaptation of NHE-3 in the rat thick ascending limb: effects of high sodium intake and metabolic alkalosis

1999 ◽  
Vol 276 (1) ◽  
pp. F18-F26 ◽  
Author(s):  
Kamel Laghmani ◽  
Régine Chambrey ◽  
Marc Froissart ◽  
Maurice Bichara ◽  
Michel Paillard ◽  
...  
Keyword(s):  
Metabolic Alkalosis ◽  
Sodium Intake ◽  
Mrna Abundance ◽  
Thick Ascending Limb ◽  
Transport Activity ◽  
High Sodium ◽  
High Sodium Intake ◽  
Medullary Thick Ascending Limb ◽  
Linear Relationships ◽  
Dependent Cell

The present studies examined the effects of chronic NaCl administration and metabolic alkalosis on NHE-3, an apical Na+/H+exchanger of the rat medullary thick ascending limb of Henle (MTAL). NaCl administration had no effect on NHE-3 mRNA abundance as assessed by competitive RT-PCR, as well as on NHE-3 transport activity estimated from the Na+-dependent cell pH recovery of Na+-depleted acidified MTAL cells, in the presence of 50 μM Hoe-694, which specifically blocks NHE-1 and NHE-2. Two models of metabolic alkalosis were studied, one associated with high sodium intake, i.e., NaHCO3 administration, and one not associated with high sodium intake, i.e., chloride depletion alkalosis (CDA). In both cases, the treatment induced a significant metabolic alkalosis that was associated with a decrease in NHE-3 transport activity (−27% and −25%, respectively). Negative linear relationships were observed between NHE-3 activity and plasma pH or bicarbonate concentration. NHE-3 mRNA abundance and NHE-3 protein abundance, assessed by Western blot analysis, also decreased by 35 and 25%, respectively, during NaHCO3-induced alkalosis, and by 47 and 33%, respectively, during CDA. These studies demonstrate that high sodium intake has per se no effect on MTAL NHE-3. In contrast, chronic metabolic alkalosis, regardless of whether it is associated with high sodium intake or not, leads to an appropriate adaptation of NHE-3 activity, which involves a decrease in NHE-3 protein and mRNA abundance.

ALTERATIONS OF ALDOSTERONE BIOSYNTHESIS BY RAT ADRENAL TISSUE DUE TO INCREASED INTAKE OF SODIUM AND POTASSIUM

1968 ◽  
Vol 58 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Adrenal Glands ◽  
Sodium Intake ◽  
Potassium Ions ◽  
High Potassium ◽  
High Sodium ◽  
Potassium Intake ◽  
High Sodium Intake ◽  
Test Conditions ◽  
Sodium And Potassium

ABSTRACT Three groups of rats received respectively the following drinking fluids for two weeks: sucrose 5%; NaCl 0.154 m + sucrose; KCl 0.154 m+ sucrose. Aldosterone biosynthesis by quartered adrenal glands of these animals was studied under various in vitro conditions. Adrenals from rats drinking sucrose alone produced significantly more aldosterone under all conditions of incubation than adrenals from rats drinking NaCl, which produced more corticosterone and deoxycorticosterone. Tissue from animals drinking NaCl converted less unlabelled progesterone, 11β-hydroxyprogesterone, deoxycorticosterone and corticosterone to aldosterone and incorporated less tritiated pregnenolone, progesterone, deoxycorticosterone and corticosterone into aldosterone. Adrenals from rats drinking KCl produced less aldosterone than adrenals from rats drinking sucrose under basal conditions but not under stimulation by ACTH or potassium ions. In both groups, the production of corticosterone and of deoxycorticosterone was the same under various test conditions. These results indicate that a high sodium intake inactivates one or both enzymes essential for the conversion of corticosterone to aldosterone, whereas a high potassium intake has no significant effect on these later steps of aldosterone biosynthesis.

Functional roles of apical membrane Na+/H+ exchange in rat medullary thick ascending limb

1996 ◽  
Vol 270 (4) ◽  
pp. F691-F699 ◽  
Author(s):  
D. W. Good ◽  
B. A. Watts
Keyword(s):  
Steady State ◽  
Apical Membrane ◽  
Important Determinant ◽  
Basolateral Membrane ◽  
Thick Ascending Limb ◽  
Functional Roles ◽  
Medullary Thick Ascending Limb ◽  
Apical Membranes ◽  
Exchange Activity

The medullary thick ascending limb (MTAL) of the rat actively absorbs both HCO3- and ammonium. The roles of apical membranes Na+/H+ exchange in these processes and in determining steady-state intracellular pH (pHi) were examined in MTAL perfused in vitro with solutions containing 146 mM Na+ and 25 mM HCO3- (pH 7.4). Addition of 1 mM amiloride or 50 microM ethylisopropylamiloride (EIPA) to the lumen decreased HCO3- absorption (JHCO3) from 10.6 +/- 0.5 to 2.3 +/- 0.3 pmol.min-1.mm-1 (P < 0.001) and pHi from 7.10 +/- 0.02 to 6.86 +/- 0.03 (P < 0.001). The combination of lumen Na+ replacement plus amiloride abolished JHCO3. Chronic metabolic acidosis (CMA) caused a 32% increase in JHCO3 that was inhibited by luminal amiloride. Addition of 4 mM NH4Cl to perfusate and bath markedly decreased pHi (from 7.10 to 6.70) but did not stimulate luminal H+ secretion as assessed by HCO3- absorption. With 4 mM NH4Cl in perfusate and bath, luminal addition of amiloride decreased pHi from 6.70 +/- 0.06 to 6.50 +/- 0.05 (P < 0.005) but had no effect on net ammonium absorption. These results demonstrate that 1) apical membrane Na+/H+ exchange mediates virtually all of HCO3- absorption and is an important determinant of steady-state pHi in the MTAL; 2) the adaptive increase in HCO3- absorption in CMA is mediated by an increase in apical membrane Na+/H+ exchange; 3) ammonium markedly acidifies the cells but does not stimulate luminal acidification, suggesting that pHi is not a predominant influence on apical Na+/H+ exchange activity and that H+ generated in the cells as the result of transcellular ammonium absorption is extruded across the basolateral membrane; and 4) apical membrane Na+/H+ exchange is not important for ammonium absorption.

scholarly journals Is socio-demographic status, body mass index, and consumption of food away from home associated with high sodium intake among adults in Malaysia?: findings from the Malaysian Community Salt Survey (MyCoSS)

2021 ◽  
Vol 40 (S1) ◽  
Author(s):  
Ruhaya Salleh ◽  
Shubash Shander Ganapathy ◽  
Norazizah Ibrahim Wong ◽  
Siew Man Cheong ◽  
Mohamad Hasnan Ahmad ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Logistic Regression ◽  
Body Mass ◽  
Sodium Intake ◽  
Daily Intake ◽  
Dietary Sodium ◽  
Cooking Methods ◽  
High Sodium ◽  
High Sodium Intake ◽  
Meal Consumption

Abstract Background Studies have shown that having away from home meals contributes to high sodium intake among young people and those who lived in urban areas. This study aimed to determine the association between dietary sodium intake, body mass index, and away from home meal consumption behaviour among Malaysian adults. Methods MyCoSS was a cross-sectional household survey involving 1440 adults age 18 years and above. This study utilized stratified cluster sampling to obtain a nationally representative sample. Data was collected between October 2017 and March 2018. Socio-demographic information, dietary assessment using food frequency questionnaire (FFQ), and away from home meal consumption were assessed through a face-to-face interview by trained health personnel. Descriptive analysis and logistic regression were applied to identify the association of socioeconomic status and away from home meal consumption with dietary sodium intake. Results A total of 1032 participants completed the FFQ, with a mean age of 48.8 + 15.6 years. Based on the FFQ, slightly over half of the participants (52.1%) had high sodium intake. Results showed that 43.6% of participants consumed at least one to two away from home meals per day, while 20.8% of them had their three main meals away from home. Participants aged less than 30 years old were the strongest predictor to consume more sodium (adjusted OR: 3.83; 95%CI: 2.23, 6.58) while those of Indian ethnicity had significantly lower sodium intake. Surprisingly, having three away from home meals per day was not associated with high dietary sodium intake, although a significant association (crude OR; 1.67, 95% CI: 1.19, 2.35) was found in the simple logistic regression. Obese participants were less likely to have high dietary sodium intake compared with the normal BMI participants in the final model. Conclusion Over half of the participants consumed sodium more than the recommended daily intake, especially those who consumed three away from home meals. However, there was no significant association between high sodium intake and having three away from home meals per day. The promotion of healthy cooking methods among the public must continue to be emphasized to reduce the dietary sodium intake among Malaysian adults.

scholarly journals High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT2R-MasR axis in obese Zucker rats

2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain
Keyword(s):  
Sodium Intake ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Complex Nature ◽  
Ang Ii ◽  
Pronounced Increase ◽  
High Sodium ◽  
High Sodium Intake ◽  
Obese Rats ◽  
Obese Zucker Rats

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

scholarly journals Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through a TLR4-TRIF-PI3K signaling pathway

2017 ◽  
Vol 313 (1) ◽  
pp. F103-F115 ◽  
Author(s):  
Bruns A. Watts ◽  
Thampi George ◽  
Edward R. Sherwood ◽  
David W. Good
Keyword(s):  
Bacterial Infections ◽  
Lipid A ◽  
Thick Ascending Limb ◽  
Akt Inhibitor ◽  
Erk Activation ◽  
Akt Phosphorylation ◽  
Medullary Thick Ascending Limb ◽  
Monophosphoryl Lipid A ◽  
Monophosphoryl Lipid

Monophosphoryl lipid A (MPLA) is a detoxified derivative of LPS that induces tolerance to LPS and augments host resistance to bacterial infections. Previously, we demonstrated that LPS inhibits [Formula: see text] absorption in the medullary thick ascending limb (MTAL) through a basolateral Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-ERK pathway. Here we examined whether pretreatment with MPLA would attenuate LPS inhibition. MTALs from rats were perfused in vitro with MPLA (1 µg/ml) in bath and lumen or bath alone for 2 h, and then LPS was added to (and MPLA removed from) the bath solution. Pretreatment with MPLA eliminated LPS-induced inhibition of [Formula: see text] absorption. In MTALs pretreated with MPLA plus a phosphatidylinositol 3-kinase (PI3K) or Akt inhibitor, LPS decreased [Formula: see text] absorption. MPLA increased Akt phosphorylation in dissected MTALs. The Akt activation was eliminated by a PI3K inhibitor and in MTALs from TLR4−/−or Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β (TRIF)−/−mice. The effect of MPLA to prevent LPS inhibition of [Formula: see text] absorption also was TRIF dependent. Pretreatment with MPLA prevented LPS-induced ERK activation; this effect was dependent on PI3K. MPLA alone had no effect on [Formula: see text] absorption, and MPLA pretreatment did not prevent ERK-mediated inhibition of [Formula: see text] absorption by aldosterone, consistent with MPLA's low toxicity profile. These results demonstrate that pretreatment with MPLA prevents the effect of LPS to inhibit [Formula: see text] absorption in the MTAL. This protective effect is mediated directly through MPLA stimulation of a TLR4-TRIF-PI3K-Akt pathway that prevents LPS-induced ERK activation. These studies identify detoxified TLR4-based immunomodulators as novel potential therapeutic agents to prevent or treat renal tubule dysfunction in response to bacterial infections.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

[OP.8B.08] HIGH SODIUM INTAKE IN TREATED BUT UNCONTROLLED HYPERTENSIVE PATIENT

2017 ◽  
Vol 35 ◽  
pp. e89
Author(s):  
M. Rhee ◽  
J. Kim ◽  
S. Shin ◽  
D. Nah ◽  
N. Gu ◽  
...  
Keyword(s):  
Hypertensive Patient ◽  
Sodium Intake ◽  
High Sodium ◽  
High Sodium Intake

Renal and cardiac oxidative/nitrosative stress in salt-loaded pregnant rat

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitrosative Stress ◽  
Gestational Hypertension ◽  
Sodium Intake ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
Arterial Blood ◽  
Cardiac Ventricle

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

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