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At least 19 recordsLinked to original sources
PubMed1984

Indomethacin and angiotensin II pressor responsiveness: importance of dietary sodium.

Dietary sodium intake alters pressor responsiveness to angiotensin II (AII) as well as altering prostaglandin production. As a result, the effect of prostaglandin synthesis inhibition on the pressor responsiveness to AII was evaluated. Prostaglandin synthesis inhibition with meclofenamate (5 mg/kg) or indomethacin (5 mg/kg) significantly enhanced the pressor response for AII at infusion rates of 0.10, 0.30 and 1.0 microgram/kg per min (P less than 0.05) in rats previously on a low sodium intake but had no effect in rats previously on a high sodium intake. In low sodium intake rats, pretreatment with captopril (1 mg/kg) prevented the enhancing effect of indomethacin on angiotensin II pressor responsiveness. The pressor response for norepinephrine was unaltered by sodium intake or prostaglandin inhibition. These results suggest that prostaglandin synthetase inhibition may enhance the pressor response for angiotensin II in situations where endogenous angiotensin II levels are elevated (i.e. low sodium intake). In situations where angiotensin II levels are suppressed (i.e. captopril pretreatment or high salt intake), prostaglandin synthetase inhibitors have no effect on the pressor response to exogenous angiotensin II.

Angiotensin II↗
PubMed2004

Up-regulation of activated macrophages in response to degeneration in the taste system: effects of dietary sodium restriction.

Dietary sodium restriction combined with unilateral chorda tympani nerve section leads to a rapid and specific decrease in neurophysiological taste responses to sodium in the contralateral, intact chorda tympani (Hill and Phillips [1994] J. Neurosci. 14:2904-2910). Previous work demonstrated that dietary sodium restriction may induce these early functional deficits by inhibiting immune activity after denervation (Phillips and Hill [1996] Am. J. Physiol. 271:R857-R862). However, little is known about the leukocyte response to denervation of taste buds in fungiform papillae. In the current study, it was hypothesized that T cells and macrophages are increased in the tongue after unilateral denervation in control-fed but not sodium-restricted animals. Adult, specified pathogen-free rats received unilateral chorda tympani nerve section or sham section followed by dietary sodium restriction or maintenance on control diet. At day 1, 2, 5, 7, or 50 postsectioning, immunostaining was used to detect the percentage of staining for activated macrophages, the number of alpha beta T cells, and the number of delta gamma epithelial T cells in the tongue. The number of lingual T cells did not significantly differ between treatment groups following denervation. However, there was a dramatic bilateral increase in ED1(+) staining for activated macrophages in control-fed rats that peaked at day 2 postsectioning. In contrast, sodium-restricted rats did not show an increase in activated macrophages above baseline at any time postsectioning. Further analysis of extralingual macrophages indicated that the deficit in immune activity in sodium-restricted rats is localized to the tongue and is not widespread. A model for immune modulation of taste receptor cell function is proposed based on these novel findings.

Analysis of Variance↗
PubMed1990

The response of atrial natriuretic factor and sodium excretion to dietary sodium challenges in patients with chronic liver disease.

Despite intensive investigation, the pathogenesis of sodium retention in patients with chronic liver disease is not fully known. We have studied 19 chronic liver disease patients, 13 without (group 1) and six with (group 2) histories of clinical sodium retention (ascites or edema) by varying dietary sodium intake. The patients were placed on a 20 mmol/day constant diet for 1 wk, followed by a constant 100 mmol/day sodium diet for 1 wk under strict metabolic conditions. After 5 days of equilibration on each diet, blood and urine samples were collected for plasma atrial natriuretic factor levels and urinary sodium excretion. Group 1 patients (n = 6) achieved near sodium balance in 5 days on both a 20-mmol (urinary sodium output = 17 +/- 3 mmol/day) and a 100-mmol sodium diet (urinary sodium output = 80 +/- 5 mmol/day). Atrial natriuretic factor levels in these patients tended to be elevated, but the increase was not significantly greater than that in normal control subjects (10 +/- 4 pg/ml to 19 +/- 4 pg/ml) on the same diets. In contrast, group 2 patients (n = 5) were in significant positive sodium balance on both the 20 mmol/day sodium diet (mean urinary sodium output = 9.5 +/- 3.3 mol/day) and the 100 mmol/day sodium diet (urinary sodium output = 37 +/- 13 mmol/day). This occurred despite significantly elevated baseline atrial natriuretic factor levels and a significant increase in plasma atrial natriuretic factor levels after sodium challenge (62 +/- 9 pg/ml, p less than 0.05) on a 100 mmol/day sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗
PubMed2001

Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group.

BACKGROUND: The effect of dietary composition on blood pressure is a subject of public health importance. We studied the effect of different levels of dietary sodium, in conjunction with the Dietary Approaches to Stop Hypertension (DASH) diet, which is rich in vegetables, fruits, and low-fat dairy products, in persons with and in those without hypertension. METHODS: A total of 412 participants were randomly assigned to eat either a control diet typical of intake in the United States or the DASH diet. Within the assigned diet, participants ate foods with high, intermediate, and low levels of sodium for 30 consecutive days each, in random order. RESULTS: Reducing the sodium intake from the high to the intermediate level reduced the systolic blood pressure by 2.1 mm Hg (P<0.001) during the control diet and by 1.3 mm Hg (P=0.03) during the DASH diet. Reducing the sodium intake from the intermediate to the low level caused additional reductions of 4.6 mm Hg during the control diet (P<0.001) and 1.7 mm Hg during the DASH diet (P<0.01). The effects of sodium were observed in participants with and in those without hypertension, blacks and those of other races, and women and men. The DASH diet was associated with a significantly lower systolic blood pressure at each sodium level; and the difference was greater with high sodium levels than with low ones. As compared with the control diet with a high sodium level, the DASH diet with a low sodium level led to a mean systolic blood pressure that was 7.1 mm Hg lower in participants without hypertension, and 11.5 mm Hg lower in participants with hypertension. CONCLUSIONS: The reduction of sodium intake to levels below the current recommendation of 100 mmol per day and the DASH diet both lower blood pressure substantially, with greater effects in combination than singly. Long-term health benefits will depend on the ability of people to make long-lasting dietary changes and the increased availability of lower-sodium foods.

Blood Pressure↗
PubMed1998

Detrimental effect of dietary sodium and beneficial effect of dietary magnesium on glomerular changes in cyclosporin-A-treated spontaneously hypertensive rats.

BACKGROUND: Cyclosporin A (CsA) causes renal magnesium wasting, hypertension, and occasionally irreversible renal damage. We examined the effect of dietary sodium and magnesium on renal histology in spontaneously hypertensive rats (SHR) receiving CsA. METHODS: Forty-six 8-week-old SHR were divided into six groups and given different dietary levels of sodium (low 0.3%, high 2.6%) and magnesium (low 0.2%, high 0.6%). Low-dose CsA (5 mg/kg/d) was given subcutaneously for 6 weeks in four groups. Systolic blood pressure, serum creatinine, degree of proteinuria, and renal tissue CsA and calcium concentrations were determined. Kidney wet weight to total body-weight ratio was calculated as an index of renal hypertrophy. Renal histological alterations were scored according to glomerular changes: 100 glomeruli were assigned for severity of change a score from 0 to 3. The number of affected glomeruli was multiplied by the damage score to obtain a damage index. RESULTS: In the CsA-treated high-sodium diet group systolic blood pressure and glomerular damage index were increased, and renal hypertrophy was the most common. These changes were prevented by oral magnesium supplementation. The glomerular damage index correlated positively with increases in systolic blood pressure, serum creatinine, proteinuria, and renal calcium concentration. CONCLUSIONS: Dietary sodium enhanced CsA-induced functional and morphological renal changes in SHR and aggravated hypertensive renal arteriolar and glomerular lesions. Dietary magnesium supplementation protected against the deleterious effects of sodium and CsA.

Animals↗
PubMed2000

Urinary prostaglandin excretion in pregnancy: the effect of dietary sodium restriction.

INTRODUCTION: Dietary sodium restriction results in activation of the renin-angiotensin-aldosterone-system. In the non-pregnant situation renin release in response to a low sodium diet is mediated by prostaglandins. We studied the effect of dietary sodium restriction on urinary prostaglandin metabolism in pregnancy. PATIENTS AND METHODS: In a randomized, longitudinal study the excretion of urinary metabolites of prostacyclin (6-keto-PGF(1 alpha)and 2,3-dinor-6-keto-PGF(1 alpha)) and thromboxane A(2)(TxB(2)and 2,3-dinor-TxB(2)) was determined throughout pregnancy and post partum in 12 women on a low sodium diet and in 12 controls. RESULTS: In pregnancy the excretion of all urinary prostaglandins is increased. The 6-keto-PGF(1 alpha)/ TxB(2)-ratio as well as the 2, 3-dinor-6-keto-PGF(1 alpha)/ 2,3-dinor-TxB(2)-ratio did not significantly change in pregnancy. CONCLUISION Prostacyclin and thromboxane do not seem to play an important role in sodium balance during pregnancy.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Long-term elevations of dietary sodium produce parallel increases in the renal excretion of urodilatin and sodium.

The effects of dietary sodium intake on the renal excretion of urodilatin and of sodium were examined in six healthy male subjects. The 24-day study period was divided into three phases of 8 days each. Subjects ingested 2.8 mequiv sodium (kg body weight)-1 day-1 during the first phase, 5.6 mequiv (kg body weight)-1 day-1 during the second phase, and 8.4 mequiv (kg body weight)-1 day-1 during the third phase. The excretion of both sodium (P < 0.002) and urodilatin (P < 0.006) increased in response to the increasing dietary sodium, while urine flow did not change. Urinary urodilatin excretion correlated closely with renal sodium excretion (P < 0.001). Serum aldosterone levels (P < 0.01) as well as serum renin levels (P < 0.05) significantly decreased with increasing sodium intake. Plasma [Arg]vasopressin levels increased significantly (P < 0.05). Plasma atrial natriuretic factor and cGMP levels as well as urinary cGMP excretion rates were unaltered by the changes in sodium intake. We conclude from these results that the renal natriuretic peptide, urodilatin, but not the main cardiac member of the natriuretic peptide family may be involved in the regulation of day-to-day sodium balance.

Adult↗
PubMed1997

Renal adaptation to dietary sodium restriction and loading in rats treated neonatally with enalapril.

Neonatal treatment of rats with angiotensin-converting enzyme inhibitors or the angiotensin II type 1 receptor antagonist losartan induces irreversible renal histological abnormalities, mainly papillary atrophy, in association with an impairment in urinary concentrating ability. In the present study, sodium and potassium balance were assessed during high and low sodium intake and dietary potassium restriction in adult Wistar rats treated neonatally with enalapril (10 mg x kg(-1) x day(-1)) from 3 to 24 days of age. During balance studies, neonatally enalapril-treated rats showed 1) normal adaptation to dietary sodium restriction, 2) sodium retention during dietary sodium loading, and 3) a transient, modest, renal potassium wastage during dietary potassium restriction. Renal clearance determinations under pentobarbital anesthesia showed elevated fractional excretions of sodium and potassium and osmolar clearance without changes in glomerular filtration rate or effective renal plasma flow in enalapril-treated compared with vehicle-treated rats. Thus, in addition to the impaired urinary concentrating ability, adult rats treated neonatally with enalapril demonstrated alterations in renal sodium and potassium handling, which may be related to the prevailing papillary atrophy.

Adaptation, Physiological↗
PubMed2000

Lack of functional and morphological susceptibility of the greater superficial petrosal nerve to developmental dietary sodium restriction.

Restriction of dietary sodium during gestation has major effects on taste function and anatomy in the offspring. The chorda tympani nerve of offspring that are maintained on sodium-reduced chow throughout life (NaDep) has reduced neurophysiological responses to sodium and altered morphology of its terminal field in the nucleus of the solitary tract. There are many anatomical and physiological similarities between the chorda tympani nerve that innervates taste buds on the anterior tongue and the greater superficial petrosal nerve (GSP) that innervates taste buds on the palate. To determine if the GSP is similarly susceptible to the effects of dietary sodium restriction, the present study examined neurophysiological responses and the terminal field of the GSP in NaDep and control rats. Neurophysiological responses of the GSP to a variety of sodium and non-sodium stimuli did not differ between NaDep and control rats. Furthermore, the volume and shape of the GSP terminal field in the nucleus of the solitary tract did not differ between the groups. Therefore, despite the high degree of functional and anatomical correspondence between the chorda tympani nerve and the GSP, the GSP does not appear to be susceptible to the effects of lifelong dietary sodium restriction.

Amiloride↗
PubMed1990

Time-course and relationship of the early changes in renal sodium excretion and aldosterone secretion during dietary sodium restriction in normal man.

1. The fall in renal sodium excretion after dietary sodium restriction is prompt and reproducible. The importance of increased aldosterone secretion during the early phase (within 48 h) of this response is unclear. Using two indirect measures of aldosterone secretion (in urine and saliva), we have tried to relate changes in excretion and concentration of this hormone to renal sodium excretion during the abrupt transition from a normal (approximately 150 mmol/day) or high (260 mmol/day) to a low (5-25 mmol/day) sodium intake in 11 and seven male volunteers, respectively. 2. All subjects showed reduced renal sodium excretion within 36 h of dietary restriction, but the times at which increases in renal aldosterone excretion, saliva aldosterone concentration and plasma renin activity became statistically significant varied widely (8-72 h, 2.5- greater than 62.5 h and less than 4- greater than 38 h for renal aldosterone secretion, saliva aldosterone concentration and plasma renin activity, respectively). Circadian fluctuations in saliva aldosterone concentration were apparent and increased in amplitude during sodium restriction. 3. Urine flow rate tended to increase on the first day of sodium restriction and this reached statistical significance in the group initially on a high sodium intake (64.0 +/- 8.8 to 84.3 +/- 11.2 ml/h, P less than 0.01); although the pattern of urine flow did correlate with plasma arginine vasopressin concentration (r = -0.49, P less than 0.01), there was no significant decrease in mean plasma arginine vasopressin concentration [1.15 (0.92-1.44) to 0.90 (0.72-1.12) pmol/l, P = 0.08; geometric mean and 95% confidence limits].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Dietary sodium intake: a determinant of postprandial plasma sodium concentration in the dog.

1. The effect of dietary sodium intake on pre- and post-prandial plasma sodium concentrations and on the pattern of sodium and potassium excretion was determined in conscious female dogs, who were allowed free access to water and were fed on commercial low sodium diets supplemented with 0, 50, 100 or 250 mmol of sodium chloride/day for 6 days. 2. The preprandial plasma sodium concentration was not altered by the dietary sodium intake. However, the 4 h postprandial plasma sodium concentration was linearly related to the magnitude of dietary sodium intake, whereas the 8 h postprandial plasma sodium concentration was elevated only in dogs receiving 250 mmol of sodium/day. 3. The (0-8 h/0-24 h) ratio for urinary sodium excretion was significantly correlated with both the dietary sodium intake and the postprandial increase in plasma sodium concentration. 4. The 24 h excretion of potassium was not markedly affected by the dietary sodium intake; however, the (0-8 h/0-24 h) ratio for potassium excretion was significantly correlated with both the dietary sodium intake and the (0-8/0-24 h) ratio for sodium excretion. 5. These data indicate that: (a) postprandial increases in plasma sodium concentration need to be considered when evaluating the mechanisms involved in the daily regulation of sodium balance; (b) the daily pattern of potassium excretion is closely linked to the dietary sodium intake.

Animals↗
PubMed2006

Dietary sodium intake modulates myocardial relaxation responsiveness to angiotensin II.

Dietary sodium alters renovascular responsiveness to angiotensin II (Ang II) in normal subjects. Evidence supports a connection among dietary sodium, the rennin-angiotensin system, and myocardial function. The authors hypothesized that a similar relationship would exist in the heart, and that the pattern of responses would be qualitatively similar to the renal vasculature. Thirteen healthy volunteers (aged 38.6 +/- 4 years) entered a 2 week crossover design study (week 1, high sodium diet [HS] > 200 mmol Na/day; week 2, low sodium diet [LS], < 10 mmol Na/day) to investigate the influence of dietary sodium and Ang II on myocardial relaxation and renal blood flow (RBF). At the end of each study week, the authors assessed diastolic function (myocardial relaxation velocities [E'] using tissue Doppler imaging) and RBF (para-aminohippurate clearance) at baseline and after infusion of Ang II (3 ng/kg/min x 45 min). On HS diet, E' and RBF were higher than on LS diet (E' 14.0 +/- 1.2 vs 12.6 +/- 1.0 cm/s, P = 0.02; RBF 596 +/- 24 vs 563 +/- 26 mL/min, P = 0.02). Dietary sodium significantly modulated E' and RBF responsiveness to Ang II infusion in like manner. HS was associated with increased responsiveness compared with a blunted LS response (HS DeltaE' -1.4 +/- 0.4 cm/s vs LS DeltaE' -0.1 +/- 0.3 cm/s, P = 0.02; HS DeltaRBF -135.2 +/- 13.2 vs LS DeltaRBF -62.5 +/- 10.1 mL/min, P < 0.01). The authors describe for the first time that dietary sodium modulates myocardial relaxation and responsiveness to Ang II. It is important to consider dietary sodium intake when assessing diastolic function. Ang II may play a role in the interaction between dietary sodium and myocardial relaxation. Future research will investigate whether abnormalities in these mechanisms play a role in disorders of diastolic function.

Adult↗
PubMed1986

Relationship between sodium clearance and proximal tubular fluid output in conscious unoperated rats adapted to different dietary sodium contents.

The relationship between the proximal tubular fluid output (Vprox) and the sodium clearance (CNa) was examined in conscious unoperated diabetes insipidus rats adapted to different dietary sodium contents ranging from 5 to 300 mmol/kg. The lithium clearance (CLi) and the urine flow (V) were used as measures of Vprox, CLi being equal to and V being about one-third of Vprox. Variations in the dietary sodium content had almost no influence on CLi and V. However, repeated 2-hour clearance measurements on different days in the same rat showed considerable intraindividual variations of CLi and V, and at each dietary sodium level CNa was linearly correlated to CLi (r = 0.83-0.90) and to V (r = 0.57-0.89). Errors in bladder emptying could not explain these correlations. The slopes of the regression lines increased with increasing dietary sodium content, and the regression lines all intercepted the abscissa at approximately the same value of CLi, i.e. on the average about 40 microliter/min./100 g body weight. The results suggest that Vprox is almost independent of the dietary sodium content. Spontaneous intraindividual variation of Vprox is considerable and is associated with linearly related variation of CNa. The change of CNa for a given change of Vprox increases with the dietary sodium content.

Animals↗
PubMed2006

Benefits of and barriers to dietary sodium adherence.

Failure to limit dietary sodium leads to thirst, large fluid weight gain, and poor outcomes in patients receiving hemodialysis. Perceived benefits and barriers may influence adherence; however, tools measuring these relationships are not available. This study's purpose, based on the health belief model, was to evaluate the reliability and validity of the Beliefs about Dietary Compliance Scale (BDCS), describe perceived benefits and barriers over time, and identify individual benefits and barriers that may be amenable to tailored interventions. A convenience sample of 229 completed the BDCS at baseline. One week after baseline, 52 participants completed the BDCS to assess test-retest reliability. Four months after baseline, 187 participants (81%) remained. Cronbach's alphas for the scale ranged from .66 to .81. One-week test-retest reliabilities ranged from .68 to .86. Factor structure was supported by factor analysis. Scores remained stable over time. Barriers to dietary sodium limitations were common and more in need of intervention.

Adolescent↗
PubMed1991

Sodium appetite in rats after prolonged dietary sodium deprivation: a sexually dimorphic phenomenon.

Little sodium appetite is observed when rats are deprived of dietary sodium for several days, presumably because aldosterone secretion minimizes renal sodium losses. However, the present studies indicate that when sodium deprivation is extended to 8 days, a spontaneous sodium appetite results that far exceeds urinary sodium losses during the deprivation period; indeed, adult male rats drank as much 0.5 M NaCl solution as rats ever have been reported to drink rapidly. In contrast, female rats drank much less saline after 8 days of sodium deprivation. Because of this sexual dimorphism in sodium appetite, we also studied NaCl intake in gonadectomized rats after 8 days of sodium deprivation. Both male and female gonadectomized rats drank comparable amounts of saline as intact male rats, but they consumed much less when treated with physiological amounts of estrogen during the sodium-deprivation period. These results indicate that a robust appetite for NaCl can be produced in rats by prolonged sodium deprivation and that estrogen can blunt the induced sodium appetite.

Administration, Oral↗