Mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats

2007 ◽  
Vol 292 (5) ◽  
pp. F1490-F1500 ◽  
Author(s):  
Markus Schafflhuber ◽  
Nicola Volpi ◽  
Anke Dahlmann ◽  
Karl F. Hilgers ◽  
Francesca Maccari ◽  
...  
Keyword(s):  
Binding Capacity ◽  
Dry Weight ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Sprague Dawley Rats ◽  
Low Salt ◽  
Total Body ◽  
Dietary Salt Restriction

The idea that an osmotically inactive Na+ storage pool exists that can be varied to accommodate states of Na+ retention and/or Na+ loss is controversial. We speculated that considerable amounts of osmotically inactive Na+ are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na+ reservoirs. Six-week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 wk. At their death, we separated the tissues and determined their Na+, K+, and water content. Three weeks of growth reduced the total body Na+ content relative to dry weight (rTBNa+) by 23%. This “growth-programmed” Na+ loss originated from the bone and the completely skinned and bone-removed carcasses. The Na+ loss was osmotically inactive (45–50%) or osmotically active (50–55%). In rats aged 10 wk, compared with HS, 4 wk of LS reduced rTBNa+ by 9%. This dietary-induced Na+ loss was osmotically inactive (≈50%) and originated largely from the skin, while ≈50% was osmotically active. LS for 1 wk did not reduce skin Na+ content. The mobilization of osmotically inactive skin Na+ with long-term salt deprivation was associated with decreased negatively charged skin glycosaminoglycan content and thereby a decreased water-free Na+ binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis.

Abstract 16443: Effects of Dietary Salt Intakes on Blood Pressure, Renal Function and Oxidative Stress in Rats Treated With Candesartan

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gangyi Zhu ◽  
Yanting Yu ◽  
Xiaoyan Wang
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Renal Function ◽  
Kidney Diseases ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Low Salt ◽  
Receptor Blockers ◽  
And Oxidative Stress

Candesartan is one of angiotensin II type1 receptor blockers(ARB) and commonly used as first-line antihypertensive treatment. Low salt diet is often recommended by clinicians to the patients with hypertension and kidney diseases. However,it is not clear whether salt restriction is beneficial to the patients taking ARB. In order to explore this problem, the impacts of different salt diets on blood pressure (BP),renal function and oxidative stress were determined in 2-3 months old male Sprague Dawley rats treated with candesartan. The rats were randomly divided into 4 groups fed agar-gelled food rationally with NaCl content at 0.01%, 0.8%, 2% and 4% respectively(4-7 rats/group) while all rats were intraperitoneally injected with candesartan at 1mg / kg / day for 7 days. SBP started to decline on day 2 in all except 4% NaCl groups relative to day 0 (recorded 5-6 hrs before the first injection). On day 6, systolic BP (mmHg, tail-cuff, Softron,BP-98A) was lower in 0.8% (103.7+2.3) & 0.01% (101.6+3) groups than 2% (113.5+4.1) & 4% (129.9+4.6) groups (one way ANOVA,LSD test, P<0.05) and correlated positively with food NaCl intakes (R 2 =0.9832). DBP was changed in a similar pattern as SBP. Serum creatinine (μmol/L) was higher in 0.01% group (225+39) than groups of 0.8% (1328+350), 2% (2095+242) and 4% (1576+703) while creatinine clearance (ml/day) was lower in 0.01% group (69.3+9) than groups of 0.8% (43.7+9), 2%(27.7+2) and 4%(29+0.6). In order to determine whether oxidative stress plays any role in the BP regulation and renal function maintenance, we also checked renal protein expression of ROS components. Relative to 0.8% group, renal NOXs were not altered in 0.01% group while NOX1 (145+18,% of 0.8% group), NOX2 (240+54) and NOX4 (197+41) was higher in 2% group than other groups. Mn-SOD (77+7.8), not Cu-Zn SOD, was decreased while HO1 (170+16), not HO2, was increased in 0.01% group. Renal abundance of nitrotyrosine was lower in 0.01% than other groups indicating a decreased oxidative stress, possibly caused by increase in HO1. We concluded that salt restriction with candesartan is beneficial to antihypertensive effect of AT1R blockade but disadvantage to maintenance of renal function. Thus, cautions to choice of low salt intakes are necessary when taking ARB agents.

scholarly journals Aldosterone Is Essential for Angiotensin II-Induced Upregulation of Pendrin

2017 ◽  
Vol 29 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Daigoro Hirohama ◽  
Nobuhiro Ayuzawa ◽  
Kohei Ueda ◽  
Mitsuhiro Nishimoto ◽  
Wakako Kawarazaki ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mineralocorticoid Receptor ◽  
Intercalated Cells ◽  
Wild Type ◽  
Dietary Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Salt Restriction ◽  
Salt Diet ◽  
Low Salt ◽  
Dietary Salt Restriction

The renin-angiotensin-aldosterone system has an important role in the control of fluid homeostasis and BP during volume depletion. Dietary salt restriction elevates circulating angiotensin II (AngII) and aldosterone levels, increasing levels of the Cl−/HCO3− exchanger pendrin in β-intercalated cells and the Na+-Cl− cotransporter (NCC) in distal convoluted tubules. However, the independent roles of AngII and aldosterone in regulating these levels remain unclear. In C57BL/6J mice receiving a low-salt diet or AngII infusion, we evaluated the membrane protein abundance of pendrin and NCC; assessed the phosphorylation of the mineralocorticoid receptor, which selectively inhibits aldosterone binding in intercalated cells; and measured BP by radiotelemetry in pendrin-knockout and wild-type mice. A low-salt diet or AngII infusion upregulated NCC and pendrin levels, decreased the phosphorylation of mineralocorticoid receptor in β-intercalated cells, and increased plasma aldosterone levels. Notably, a low-salt diet did not alter BP in wild-type mice, but significantly decreased BP in pendrin-knockout mice. To dissect the roles of AngII and aldosterone, we performed adrenalectomies in mice to remove aldosterone from the circulation. In adrenalectomized mice, AngII infusion again upregulated NCC expression, but did not affect pendrin expression despite the decreased phosphorylation of mineralocorticoid receptor. By contrast, AngII and aldosterone coadministration markedly elevated pendrin levels in adrenalectomized mice. Our results indicate that aldosterone is necessary for AngII-induced pendrin upregulation, and suggest that pendrin contributes to the maintenance of normal BP in cooperation with NCC during activation of the renin-angiotensin-aldosterone system by dietary salt restriction.

Compliance with Long-Term Dietary Salt Restriction in Hypertensive Outpatients

1994 ◽  
Vol 16 (6) ◽  
pp. 729-739 ◽  
Author(s):  
Junichiro Hashimoto ◽  
Yutaka Imai ◽  
Naoyoshi Minami ◽  
Masanori Munakata ◽  
Hiromichi Sakuma ◽  
...  
Keyword(s):  
Dietary Salt ◽  
Salt Restriction ◽  
Dietary Salt Restriction

Redistribution of distal tubule Na+-Cl− cotransporter (NCC) in response to a high-salt diet

2006 ◽  
Vol 291 (2) ◽  
pp. F503-F508 ◽  
Author(s):  
Monica B. Sandberg ◽  
Arvid B. Maunsbach ◽  
Alicia A. McDonough
Keyword(s):  
Immunoelectron Microscopy ◽  
Gradient Centrifugation ◽  
Distal Tubule ◽  
High Salt ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Sprague Dawley Rats ◽  
Low Salt

The distal convoluted tubule (DCT) apical Na+-Cl− cotransporter (NCC) is responsible for the reabsorption of 5–10% of filtered NaCl and is the target for thiazide diuretics. NCC abundance is increased during dietary NaCl restriction and by aldosterone and decreased during a high-salt (HS) diet and mineralocorticoid blockade. This study tested the hypothesis that subcellular distribution of NCC is also regulated in response to changes in dietary salt. Six-week-old Sprague-Dawley rats were fed a normal-salt diet (NS; 0.4% NaCl) for 3 wk, then switched to a HS diet (4% NaCl) for 3 wk or a low-salt diet (LS; 0.07% NaCl) for 1 wk. Under anesthesia, kidneys were excised, renal cortex was dissected, and NCC was analyzed with specific antibodies after either 1) density gradient centrifugation followed by immunoblotting or 2) fixation followed by immunoelectron microscopy. The HS diet decreased NCC abundance to 0.50 ± 0.10 of levels in LS diet (1.00 ± 0.23). The HS diet also caused a redistribution of NCC from low to higher density membranes. Immunoelectron microscopy revealed that NCC resides predominantly in the apical membrane in rats fed the LS diet and increases in subapical vesicles in rats fed the HS diet. In conclusion, a HS diet provokes a rapid and persistent redistribution of NCC from apical to subapical membranes, a mechanism that would facilitate a homeostatic decrease in NaCl reabsorption in the DCT to compensate for increased dietary salt.

scholarly journals The area postrema does not modulate the long-term salt sensitivity of arterial pressure

1998 ◽  
Vol 275 (4) ◽  
pp. R1209-R1217 ◽  
Author(s):  
John P. Collister ◽  
John W. Osborn
Keyword(s):  
Arterial Pressure ◽  
Continuous Monitoring ◽  
Area Postrema ◽  
Postoperative Recovery ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Sprague Dawley Rats ◽  
Body Fluid Homeostasis ◽  
The Given

The hindbrain circumventricular organ, the area postrema (AP), receives multiple signals linked to body fluid homeostasis. In addition to baroreceptor input, AP cells contain receptors for ANG II, vasopressin, and atrial natriuretic peptide. Hence, it has been proposed that the AP is critical in long-term adjustments in sympathetic outflow in response to changes in dietary NaCl. The present study was designed to test the hypothesis that long-term control of arterial pressure over a range of dietary NaCl requires an intact AP. Male Sprague-Dawley rats were randomly selected for lesion of the AP (APx) or sham lesion. Three months later, rats were instrumented with radiotelemetry transmitters for continuous monitoring of mean arterial pressure (MAP) and heart rate and were placed in individual metabolic cages. Rats were given 1 wk postoperative recovery. The dietary salt protocol consisted of a 7-day period of 1.0% NaCl (control), 14 days of 4.0% NaCl (high), 7 days of 1.0% NaCl, and finally 14 days of 0.1% NaCl (low). The results are reported as the average arterial pressure observed on the last day of the given dietary salt period: APx ( n = 7) 114 ± 2 (1.0%), 110 ± 3 (4.0%), 110 ± 3 (1.0%), and 114 ± 4 (0.1%) mmHg; sham ( n = 6) 115 ± 2 (1.0%), 114 ± 3 (4.0%), 111 ± 3 (1.0%), and 113 ± 2 (0.1%) mmHg. Neither group of rats demonstrated significant changes in MAP throughout the entire dietary salt protocol. Furthermore, no significant differences in MAP were detected between groups throughout the protocol. All lesions were histologically verified. These results suggest that the area postrema plays no role in long-term control of arterial pressure during chronic changes in dietary salt.

Dietary salt restriction accelerates atherosclerosis in apolipoprotein E-deficient mice

2005 ◽  
Vol 180 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Ognen Ivanovski ◽  
Dorota Szumilak ◽  
Thao Nguyen-Khoa ◽  
Michele Dechaux ◽  
Ziad A. Massy ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Dietary Salt Restriction ◽  
Deficient Mice

Long-term exposure of Sprague Dawley rats to 20 kHz triangular magnetic fields

2006 ◽  
Vol 82 (4) ◽  
pp. 285-291 ◽  
Author(s):  
H. J. Lee ◽  
S. H. Kim ◽  
S. Y. Choi ◽  
Y. M. Gimm ◽  
J. K. Pack ◽  
...  
Keyword(s):  
Magnetic Fields ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Differential Regulation of the Epithelial Sodium Channel (ENaC) in Rat Kidney, Lung and Distal Colon in Response to Aldosterone.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 724-724
Author(s):  
Shyama M E Masilamani ◽  
Gheun-Ho Kim ◽  
Mark A Knepper
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Distal Colon ◽  
Β Subunit ◽  
Dietary Salt ◽  
Α Subunit ◽  
Salt Restriction ◽  
Γ Subunit ◽  
Dietary Salt Restriction ◽  
Epithelial Sodium Channel Enac

P170 The mineralocorticoid hormone, aldosterone increases renal tubule Na absorption via increases in the protein abundances of the α-subunit of the epithelial sodium channel (ENaC) and the 70 kDa form of the γ- subunit of ENaC (JCI 104:R19-R23). This study assesses the affect of dietary salt restriction on the regulation of the epithelial sodium channel (ENaC) in the lung and distal colon, in addition to kidney, using semiquantitative immunoblotting. Rats were placed initially on either a control Na intake (0.02 meq/day), or a low Na intake (0.2 meq/day) for 10 days. The low salt treated rats demonstrated an increase in plasma aldosterone levels at day 10 (control = 0.78 + 0.32 nM; Na restricted = 3.50 + 1.30 nM). In kidney homogenates, there were marked increases in the band density of the α-subunit of ENaC (286 % of control) and the 70 kDa form of γ-subunit of ENaC (262 % of control), but no increase in the abundance of the β-subunit of ENaC. In lung homogenates, there was no significant change in the band densities of the α, β, or γ subunits of ENaC. In distal colon, there was an increase in the band density of the β-subunit of ENaC (311 % of control) and an increase in both the 85 kDa (2355% of control) and 70 kDa (843 % of control) form of the γ subunit of ENaC in response to dietary Na restriction. However, there was no significant difference in the band density of the α-subunit of ENaC. These findings demonstrate tissue specific regulation of the three subunits of ENaC in response to dietary salt restriction.

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