scholarly journals High-salt intake primes the rat kidney to respond to a subthreshold uroguanylin dose during ex vivo renal perfusion

2009 ◽  
Vol 158 (1-3) ◽  
pp. 6-13 ◽  
Author(s):  
Manassés C. Fonteles ◽  
A. Havt ◽  
Rodrigo B. Prata ◽  
Patrícia H.B. Prata ◽  
Helena S.A. Monteiro ◽  
...  
Keyword(s):  
Salt Intake ◽  
Ex Vivo ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
High Salt ◽  
High Salt Intake

Effects of high salt intake on dopamine production in rat kidney

1991 ◽  
Vol 260 (5) ◽  
pp. E675-E679 ◽  
Author(s):  
M. Hayashi ◽  
Y. Yamaji ◽  
W. Kitajima ◽  
T. Saruta
Keyword(s):  
Degradation Rate ◽  
Salt Intake ◽  
Rat Kidney ◽  
Dopamine Metabolism ◽  
High Salt ◽  
Acid Decarboxylase ◽  
Amino Acid Decarboxylase ◽  
High Salt Intake ◽  
Urinary Dopamine ◽  
Convoluted Tubules

To examine the origin of increased urinary dopamine excretion (UDAV) during high salt intake, we measured UDAV from the innervated (INN) or the chronically denervated (DEN) kidney in rats fed either a high-salt (HS) or low-salt (LS) diet. UDAV of DEN [3.50 +/- 0.46 ng. min-1.inulin clearance (CIN)-1] and INN (4.00 +/- 0.59 ng. min-1.CIN-1) kidneys in the HS group showed a significant increase compared with that of the respective kidney in the LS group (DEN 1.42 +/- 0.12, INN 1.44 +/- 0.09 ng.min-1.CIN-1), whereas the effect of denervation on UDAV was not significantly different between two groups. We determined aromatic L-amino acid decarboxylase (L-AADC) activity and dopamine degradation rate of microdissected proximal convoluted tubules to study the changes in dopamine metabolism. L-AADC activity in the HS group showed a significant increase compared with that in the LS group, although there was no significant change in dopamine degradation rate. We conclude that the increase in UDAV during high salt intake was mainly caused by the enhancement of extraneural dopamine production by the kidney in rats. Dopamine-producing enzyme, but not its degradation in the tubular cells, plays a role in the regulation of extraneural dopamine production.

scholarly journals The sodium-activated sodium channel is expressed in the rat kidney thick ascending limb and collecting duct cells and is upregulated during high salt intake

2012 ◽  
Vol 303 (1) ◽  
pp. F105-F109 ◽  
Author(s):  
Lucienne S. Lara ◽  
Ryousuke Satou ◽  
Camille R. T. Bourgeois ◽  
Alexis A. Gonzalez ◽  
Andrea Zsombok ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Salt Intake ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Extracellular Fluid ◽  
High Salt ◽  
Thick Ascending Limb ◽  
Principal Cells ◽  
High Salt Intake

Increased dietary salt triggers oxidative stress and kidney injury in salt-sensitive hypertension; however, the mechanism for sensing increased extracellular Na+ concentration ([Na+]) remains unclear. A Na+-activated Na+ channel (Na sensor) described in the brain operates as a sensor of extracellular fluid [Na+]; nonetheless, its presence in the kidney has not been established. In the present study, we demonstrated the gene expression of the Na sensor by RT-PCR and Western blotting in the Sprague-Dawley rat kidney. Using immunofluorescence, the Na sensor was localized to the luminal side in tubular epithelial cells of collecting ducts colocalizing with aquaporin-2, a marker of principal cells, and in thick ascending limb, colocalizing with the glycoprotein Tamm-Horsfall. To determine the effect of a high-salt diet (HSD) on Na sensor gene expression, we quantified its transcript and protein levels primarily in renal medullas from control rats and rats subjected to 8% NaCl for 7 days ( n = 5). HSD increased Na sensor expression levels (mRNA: from 1.2 ± 0.2 to 5.1 ± 1.3 au; protein: from 0.98 ± 0.15 to 1.74 ± 0.28 au P < 0.05) in the kidney medulla, but not in the cortex. These data indicate that rat kidney epithelial cells of the thick ascending limb and principal cells of the collecting duct possess a Na sensor that is upregulated by HSD, suggesting an important role in monitoring changes in tubular fluid [Na+].

scholarly journals High salt intake induces collecting duct HDAC1-dependent NO signaling

2020 ◽  
Author(s):  
Randee S Sedaka ◽  
Kelly A. Hyndman ◽  
Elena Mironova ◽  
James D Stockand ◽  
Jennifer S Pollock
Keyword(s):  
Salt Intake ◽  
Ex Vivo ◽  
Collecting Duct ◽  
High Salt ◽  
No Production ◽  
Mrna Levels ◽  
No Donor ◽  
Histone Deacetylase 1 ◽  
High Salt Intake ◽  
Endothelin B

We reported that high salt intake stimulates renal collecting duct (CD) endothelin B receptor (ETBR)/NOS1β-dependent NO production inhibiting the epithelial sodium channel (ENaC) promoting natriuresis. However, the mechanism underlying the high salt (HS) induced increase of NO production is unclear. Histone deacetylase 1 (HDAC1) responds to increased fluid flow, as can occur in the CD during HS intake. The renal inner medulla (IM), in particular the IMCD, has the highest NOS1 activity within the kidney. Hence, we hypothesized that HS intake provokes HDAC1 activation of NO production in the IM. HS intake for one week significantly increased HDAC1 abundance in the IM. Ex vivo treatment of dissociated IM from HS mice with a selective HDAC1 inhibitor (MS-275) decreased NO production with no change in endothelin-1 (ET-1) peptide or mRNA levels. We further investigated the role of the ET-1/ETBR/NOS1β signaling pathway with chronic ETBR blockade (A-192621). Although NO was decreased and ET-1 levels were elevated in dissociated IM from HS mice treated with A-192621, ex vivo MS-275 did not further change NO or ET-1 levels suggesting that HDAC1 mediated NO production is regulated at the level or downstream of ETBR activation. In split-open CDs from HS mice, patch clamp analysis revealed significantly higher ENaC activity after MS-275 pretreatment, which was abrogated by an exogenous NO donor. Moreover, flow-induced increases in mIMCD-3 cell NO production were blunted by HDAC1 or calcium inhibition. Taken together, these findings indicate that HS intake induces HDAC1-dependent activation of the ETBR/NO pathway contributing to the natriuretic response.

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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