Flow-dependent arteriolar dilation in normotensive rats fed low- or high-salt diets

1995 ◽  
Vol 269 (4) ◽  
pp. H1407-H1414 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Vessel Occlusion ◽  
High Salt Intake ◽  
Significant Difference ◽  
Low Salt ◽  
No Release ◽  
Luminal Flow ◽  
Arteriolar Tone

Ingestion of a high-salt diet has previously been shown to suppress the endogenous influence of nitric oxide (NO) on arteriolar tone in hypertension-resistant, salt-resistant Dahl (SR/Jr) rats. Because luminal blood flow can be an important stimulus for endothelial NO release, this study was undertaken to determine whether high salt intake can also lead to a deficit in the direct flow-dependent regulation of arteriolar diameter. The spinotrapezius muscle microvasculature was studied by in vivo microscopy in SR/Jr rats fed low (0.45%)- or high (7%)-salt diets for 2 wk, and arcade arteriole responses to increased luminal flow (via parallel vessel occlusion) were studied in both dietary groups. There was no significant difference between groups in arterial pressure or in resting arteriolar diameters, volume flows, or wall shear rates. In low-salt SR/Jr, a 36% increase in luminal flow produced an average arteriolar dilation of 38% that was significantly reduced by the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). In high-salt SR/Jr, a similar flow increase produced an average dilation of only 16% (P < 0.05 vs. low-salt SR/Jr), and this response was unaffected by L-NMMA. Inhibition of cyclooxygenase activity with meclofenamate had no effect on this response in either group. These findings suggest that NO release mediates a portion of flow-dependent arteriolar dilation in rat spinotrapezius muscle and that high salt intake, in the absence of hypertension, can attenuate this response via a suppression of NO activity.

scholarly journals High Salt Diet Impacts the Risk of Sarcopenia Associated with Reduction of Skeletal Muscle Performance in the Japanese Population

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3474
Author(s):  
Yasuko Yoshida ◽  
Keisei Kosaki ◽  
Takehito Sugasawa ◽  
Masahiro Matsui ◽  
Masaki Yoshioka ◽  
...  
Keyword(s):  
Older People ◽  
Salt Intake ◽  
Handgrip Strength ◽  
High Salt ◽  
Muscle Performance ◽  
World Health ◽  
Fat Percentage ◽  
High Salt Intake ◽  
Significant Difference ◽  
Low Salt

The World Health Organization has recommended 5 g/day as dietary reference intakes for salt. In Japan, the averages for men and women were 11.0 g/day and 9.3 g/day, respectively. Recently, it was reported that amounts of sodium accumulation in skeletal muscles of older people were significantly higher than those in younger people. The purpose of this study was to investigate whether the risk of sarcopenia with decreased muscle mass and strength was related to the amount of salt intake. In addition, we investigated its involvement with renalase. Four groups based on age and salt intake (“younger low-salt,” “younger high-salt,” “older low-salt,” and “older high-salt”) were compared. Stratifying by age category, body fat percentage significantly increased in high-salt groups in both younger and older people. Handgrip strength/body weight and chair rise tests of the older high-salt group showed significant reduction compared to the older low-salt group. However, there was no significant difference in renalase concentrations in plasma. The results suggest that high-salt intake may lead to fat accumulation and muscle weakness associated with sarcopenia. Therefore, efforts to reduce salt intake may prevent sarcopenia.

scholarly journals Eplerenone inhibits aldosterone-induced renal expression of cyclooxygenase

2012 ◽  
Vol 13 (3) ◽  
pp. 353-359 ◽  
Author(s):  
MA Bayorh ◽  
A Rollins-Hairston ◽  
J Adiyiah ◽  
D Lyn ◽  
D Eatman
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Prostaglandin E ◽  
Renal Tubules ◽  
Protective Effects ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Low Salt ◽  
Cox 2

Introduction: The upregulation of cyclooxygenase (COX) expression by aldosterone (ALDO) or high salt diet intake is very interesting and complex in the light of what is known about the role of COX in renal function. Thus, in this study, we hypothesize that apocynin (APC) and/or eplerenone (EPL) inhibit ALDO/salt-induced kidney damage by preventing the production of prostaglandin E2 (PGE2). Methods: Dahl salt-sensitive rats on either a low-salt or high-salt diet were treated with ALDO (0.2 mg pellet) in the presence of EPL (100 mg/kg/day) or APC (1.5 mM). Indirect blood pressure, prostaglandins and ALDO levels and histological changes were measured. Results: Cyclooxygenase-2 (COX-2) levels were upregulated in the renal tubules and peritubular vessels after high-salt intake, and APC attenuated renal tubular COX-2 protein expression induced by ALDO. Plasma PGE2 levels were significantly reduced by ALDO in the rats fed a low-salt diet when compared to rats fed a high-salt diet. PGE2 was blocked by EPL but increased in the presence of APC. Conclusions: The beneficial effects of EPL may be associated with an inhibition of PGE2. The mechanism underlying the protective effects of EPL is clearly distinct from that of APC and suggests that these agents can have differential roles in cardiovascular disease.

Factors affecting Potassium Balance During Frusemide Administration

1984 ◽  
Vol 67 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William E. Mitch ◽  
Ralph A. Kelly ◽  
Paul A. Friedman ◽  
Paul F. Souney ◽  
...  
Keyword(s):  
Salt Intake ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Water Load ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt

1. We investigated the effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to six normal subjects. Subjects received 40 mg of frusemide for 3 days during three different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a fourth protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. 2. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. 3. During low salt intake, the magnitude of the acute kaliuresis following the first dose of frusemide and the slope of the linear relationship between UKV and the log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (−86 ± 7 mmol/3 days; P < 0.001). 4. Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. 5. When a water load was given concurrently with frusemide, the acute kaliuresis was >30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. 6. We conclude that: (a) K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; (b) this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; (c) the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.

Abstract 138: High Salt Intake Augments Excitability of Pre-sympathetic PVN Neurons Through Dysfunction of the Endoplasmic Reticulum Ca2+ ATPase

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Robert A Larson ◽  
Andrew D Chapp ◽  
Michael J Huber ◽  
Zixi Cheng ◽  
Zhiying Shan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Salt Intake ◽  
Sympathetic Neurons ◽  
High Salt ◽  
Ventrolateral Medulla ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Atpase Inhibitor ◽  
High Salt Intake ◽  
Significant Difference

High salt (HS) intake sensitizes pre-sympathetic neurons in the hypothalamic paraventricular nucleus (PVN) leading to augmented neuronal excitability. Recently, we reported that dysfunction of Ca 2+ dependent K + channels in the PVN contributes to HS intake induced sympathoexcitation. The endoplasmic reticulum (ER) acts as a Ca 2+ store and plays an important role in regulating intracellular Ca 2+ homeostasis. The ER Ca 2+ ATPase is responsible for maintaining the high level of ER Ca 2+ and loss of function would deplete the Ca 2+ store contributing to the reduced activity of Ca 2+ dependent K + channels. We hypothesized that a 2% (NaCl) HS diet for 5 weeks would reduce function of the ER Ca 2+ ATPase and augment excitability of PVN neurons with axon projections to the rostral ventrolateral medulla (PVN-RVLM) identified by retrograde label. In whole cell current-clamp recordings from PVN-RVLM neurons, graded current injections evoked graded increases in spike frequency. Maximum discharge was evoked by +200 pA injections and averaged 22±2 Hz (n=6) in normal salt (NS) control and was significantly augmented (p<0.05) by HS diet 34±5 Hz (n=8). Bath application of thapsigargin (TG) (0.5 μM), the ER Ca 2+ ATPase inhibitor, augmented excitability of PVN-RVLM neurons in NS (32±4 Hz, n=5, p<0.05), yet had no significant effect in HS rats (32±6 Hz, n=6). ER Ca 2+ ATPase function was assessed in whole animal preparations by bilateral PVN microinjection of TG in anesthetized rats. PVN microinjection of TG (0.15, 0.3 0.75 and 1.5 nmol/100nl) increased sympathetic nerve activity (SNA) and mean arterial pressure (MAP) in a dose-dependent manner in NS rats. Maximum increases in splanchnic SNA (SSNA), renal SNA (RSNA) and MAP elicited by PVN TG (0.75 nmol/100nl; n=5) were 93±7%, 75±7%, and 11±2mmHg, respectively. In contrast, sympathoexcitatory responses to PVN TG (0.75 nmol/100nl; n=5) were attenuated in HS treated rats (SSNA 41±8%, RSNA 22±5%, p<0.05 vs. NS) while MAP responses demonstrated no significant difference (+8±2 mmHg, p>0.05 vs NS). Our data indicate that a HS diet reduces ER Ca 2+ ATPase activity and augments excitability of PVN-RVLM neurons in vitro. Altered ER Ca 2+ homeostasis may contribute to sympathoexcitation through loss of Ca 2+ dependent K + channel activity in the PVN.

Postprandial natriuresis in humans: further evidence that urodilatin, not ANP, modulates sodium excretion

1996 ◽  
Vol 270 (2) ◽  
pp. F301-F310 ◽  
Author(s):  
C. Drummer ◽  
W. Franck ◽  
M. Heer ◽  
W. G. Forssmann ◽  
R. Gerzer ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Salt ◽  
Peak Rate ◽  
High Salt Intake ◽  
Low Salt ◽  
Chloride Excretion

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mumol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary excretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/min. The effect of high-salt intake on urinary sodium, chloride, and urodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin and sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which was acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriuretic profile, and no positive correlation between plasma ANP and sodium excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily involved in the regulation of the excretion of sodium and chloride.

scholarly journals High Salt Intake Increases Copeptin but Salt Sensitivity Is Associated with Fluid Induced Reduction of Copeptin in Women

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Irina Tasevska ◽  
Sofia Enhörning ◽  
Philippe Burri ◽  
Olle Melander
Keyword(s):  
Body Weight ◽  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
Dietary Salt ◽  
Urinary Volume ◽  
Salt Consumption ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Changes

This study investigated if copeptin is affected by high salt intake and whether any salt-induced changes in copeptin are related to the degree of salt sensitivity. The study was performed on 20 men and 19 women. In addition to meals containing 50 mmol NaCl daily, capsules containing 100 mmol NaCl and corresponding placebo capsules were administered during 4 weeks each, in random order. Measurements of 24 h blood pressure, body weight, 24 h urinary volume, and fasting plasma copeptin were performed at high and low salt consumption. Copeptin increased after a high compared to low dietary salt consumption in all subjects 3,59 ± 2,28 versus 3,12 ± 1,95 (P= 0,02). Copeptin correlated inversely with urinary volume, at both low (r= −0,42;P= 0,001) and high (r= −0,60;P< 0,001) salt consumption, as well as with the change in body weight (r= −0,53;P< 0,001). Systolic salt sensitivity was inversely correlated with salt-induced changes of copeptin, only in females (r= −0,58;P= 0,017). As suppression of copeptin on high versus low salt intake was associated with systolic salt sensitivity in women, our data suggest that high fluid intake and fluid retention may contribute to salt sensitivity.

scholarly journals SUN-LB94 Impact of the Gut Microbiome and Renin-Angiotensin-Aldosterone System in Hypertensive Patients With Low-Salt Intake

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kouki Taniguchi ◽  
Satoshi Nagase ◽  
Shigehiro Karashima ◽  
Mitsuhiro Kometani ◽  
Daisuke Aono ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiome ◽  
Salt Intake ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt ◽  
The Impact

Abstract Salt intake is one of most important environmental factors responsible for triggering the onset of hypertension. Renin-angiotensin-aldosterone system (RAAS) plays a key role in adjusting sodium homeostasis and blood pressure. Recently, the potential role of the gut microbiome (GM) in altering the health of the host has drawn considerable attention. We investigated the impact of intestinal microflora and RAAS in hypertensive patients with low-salt or high-salt intake using an observational study. A total of 239 participants were enrolled and their GMs and clinical backgrounds examined, including the renin-angiotensin-aldosterone system and inflammatory cytokine levels. On the basis of enterotypes—determined by cluster analysis—and salt intake, the participants were classified into four groups, low salt/GM enterotype 1, low salt/GM enterotype 2, high salt/GM enterotype 1, and high salt/GM enterotype 2. The prevalence of hypertension was significantly lower in the low-salt intake (low salt/GM enterotype 1 = 47% vs low salt/GM enterotype 2 = 27%, p = 0.04) groups. No significant difference in the prevalence of hypertension was observed for the two GM enterotype groups with high-salt intake (GM enterotype 1 = 50%, GM enterotype 2 = 47%; p = 0.83). Plasma aldosterone concentration was significantly different among the four groups (p &lt; 0.01). Furthermore, the relative abundance of Blautia, Bifidobacterium, Escherichia-Shigella, Lachnoclostridium, and Clostridium sensu stricto was also significantly different among these enterotypes. This suggested in certain individuals (with specific gut bacteria composition) changing dietary habits—to low salt—would be ineffective for regulating hypertension through RAAS. Our findings provide a new strategy for controlling blood pressure and preventing the development of hypertension through restoring GM homeostasis.

Abstract P207: High Salt Intake desynchronizes the Molecular Clock in Rats

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Joshua S Speed ◽  
Kelly A Hyndman ◽  
Kaehler A Roth ◽  
Malgorzata Kasztan ◽  
Jermaine G Johnston ◽  
...  
Keyword(s):  
Molecular Clock ◽  
Salt Intake ◽  
Receptor Activation ◽  
High Salt ◽  
Dietary Sodium ◽  
Expression Control ◽  
High Salt Intake ◽  
Significant Difference ◽  
A Cell ◽  
Peripheral Clocks

Circadian rhythms in physiologic functions are driven, at the molecular level, by a group of transcription factors that oscillate over a 24 hour period, collectively termed the molecular clock. Within the kidney, it has been shown that the molecular clock directly influences transcription of Na + transporters and channels, including ENaC. ENaC is regulated by endothelin-1 (ET-1), via ET B receptor activation, in response to high salt intake. Thus, we hypothesized that increases in dietary sodium regulate the renal molecular clock (which in turn would facilitate Na+ homeostasis) through an ET B dependent mechanism. To address this question, we examined the effect of high salt (HS) intake on renal clock gene ( Bmal1, Cry1, Per1, Per2 ) expression. Control and ET B receptor deficient (ET B def) rats (a model of elevated renal ENaC) were placed on either HS or normal salt (NS) for two weeks and euthanized every 4 hours beginning at Zeitgeber Time 0 (Lights on). In the inner medulla, HS causes a phase delay in Bmal1 (Fig 1A) expression in control but not ET B def rats (Fig 1B). In addition, HS suppressed the expression of Cry1 , and Per2 during the respective acrophase in both control and ET B def rats (Fig 1C-1F) with no significant effect on Per1 . In contrast, no significant difference in the expression of Bmal1, Cry1, Per2, or Per1 (Fig 1I-1P) was found in response to HS in the renal cortex of either control or ET B def. These data indicate that HS feeding desynchronizes the molecular clock within the kidney and provides evidence that peripheral clocks are regulated in a cell type specific manner, even within the same organ.

Blood pressure and fluid-electrolyte balance in mice with reduced or absent ANP

1996 ◽  
Vol 271 (1) ◽  
pp. R109-R114 ◽  
Author(s):  
S. W. John ◽  
A. T. Veress ◽  
U. Honrath ◽  
C. K. Chong ◽  
L. Peng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Volume Expansion ◽  
High Salt Intake ◽  
Low Salt

Atrial natriuretic peptide (ANP)-gene knockout mice of three genotypes (+/+, +/-, and -/-) were maintained on a low-salt diet (0.008% NaCl). They were then fed either the same low-salt diet or a high-salt diet (8% NaCl) for 1 wk. No differences were found among genotypes in daily food and water intakes or in urinary volume and electrolyte excretions. Arterial blood pressures measured in anesthetized animals at the end of the dietary regimen were significantly and similarly increased in -/- compared with +/+ mice on each diet. Renal excretion of fluid and electrolytes was measured in anesthetized mice before and after acute blood volume expansion. No genotype differences were observed before volume expansion. After volume expansion the wild-type (+/+) mice had much greater saluretic responses than either the heterozygous (+/-) or the homozygous mutant (-/-) animals on the low-salt diet but not on the high-salt diet. We conclude that ANP lowers blood pressure in the absence of detected changes in renal function; ANP is not essential for normal salt balance, even on high-salt intake; and ANP is essential for the natriuretic response to acute blood volume expansion on a low-salt but not high-salt intake.

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