Low Sodium Chloride Diet Research Articles

The Use of Diets Containing High Levels of Zinc for Controlling Early Growth in Female Broiler Chicks

A study was carried out with White Rock female chicks to evaluate the possibility of using dietary Zn supplied as ZnO, to control feed intake and weight gain during the period of 1 to 3 wk of age. The levels of supplemental Zn tested were 0, 0.25, 0.50, and 1.0% (Experiment 1); 0, 0.65, 0.75, and 0.85% (Experiment 2); 0.7 and 0.8% (Experiment 3). The effect of Zn supplementation was compared with that of a low sodium chloride diet (L-NaCl-D) and of severe feed restriction (SFR), which was calculated to supply energy only for maintenance (Experiments 1 and 3, respectively). The compensatory growth of the chicks from 3 to 4 wk of age was also evaluated.Feed intake and weight gain were negatively proportional to the levels of dietary Zn supplementation and there were significant (P < 0.02 and P < 0.01, in Experiments 1 and 2, respectively) negative correlations between supplemental dietary Zn levels and relative weight gains (values observed in the unsupplemented diet = 100%). The effects of L-NaCl-D and SFR on decreasing weight gain were calculated, according to the equations obtained in Experiments 1 and 2 to be equivalent to these of 0.58 to 0.65% and 0.78 to 0.87% Zn supplementation, respectively.Relative weight gain and feed efficiency of the chicks from 3 to 4 wk of age, after withdrawal of the growth-depressing factors, were positively related to the degree of growth depression during 1 to 3 wk of age; however, the intensity of recovery from a similar degree of growth depression induced by L-NaCl-D, SFR, or dietary Zn was least in the last mentioned treatment. It is concluded that dietary Zn supplementation can be used as an efficient tool for controlling early growth of young broiler breeder chicks.

Effects of enalapril on the hyperinsulinemic response to severe salt restriction in obese young men with mild systemic hypertension

Hypertension in obese patients is associated with hyperinsulinemia and salt sensitivity. Very low salt diets may exacerbate hyperinsulinemia, perhaps by activating the renin-angiotensin system. Therefore, the effects of a low salt diet alone and with enalapril on blood pressure and the insulin response to an oral glucose tolerance test were studied in 9 obese (body mass index 35 ± 2 kg/m 2) men with mild hypertension. Measurements were first obtained after a 2-week high-salt (20 mEq/day sodium diet + eleven 1 g salt tablets per day) baseline period. The same measurements were repeated after 2 weeks on a low salt diet (20 mEq/day) and after 2 weeks on low salt diet with enalapril in random sequence. The insulin area under the curve increased from 12.8 ± 3.0 mU-min/dl during high salt to 16.6 ± 3.2 mU-min/dl (p < 0.001). Plasma renin activity also increased with salt restriction from 1.4 ± 0.2 to 3.0 ± 0.5 ng/ml/hour, p = 0.01. With addition of enalapril to the low sodium chloride diet, the insulin area under the curve (14.5 ± 2.6 mU-min/dl) was not significantly different from that during the high sodium chloride phase. Mean blood pressure in the laboratory was 105 ± 1 mm Hg with high salt versus 99 ± 1 mm Hg with low salt, p < 0.05. Addition of enalapril to the low-salt diet reduced mean blood pressure to 87 ± 1 mm Hg (p < 0.01 vs low salt), largely by reducing total systemic resistance (p < 0.05). Salt restriction decreases laboratory BP while raising insulin levels in obese men with mild hypertension. Enalapril diminishes the hyperinsulinemic effect and enhances the hypotensive action of the low-salt diet. These findings indicate that the hyperinsulinemic effect of severe salt restriction persists for ≥2 weeks. Moreover, activation of the renin-angiotensin system may contribute to impaired insulin metabolism during very low salt diets.

Psychiatric aspects of congestive heart failure: implications for consulting psychiatrists.

Abnormalities of mental function are common problems in patients with congestive heart failure, a problem that is often referred to the consulting psychiatrist. These abnormalities become more frequent and more serious as failure of the heart progresses and they can exhibit a wide variety of manifestations. Cardiac output and cerebral blood flow are preserved due to compensatory mechanisms in mild heart failure but can be severely compromised in advanced failure. Drugs used to treat heart failure, especially digitalis, can produce a wide variety of mental aberrations including delirium, usually when these drugs are used in excess. Diuretics can produce electrolyte abnormalities resulting in mental derangements and vasodilator therapy can produce hypotension. Psychotropic drugs are well recognized as having significant cardiovascular effects that need to be considered when these agents are applied to the cardiac patient. Antidepressant and antipsychotic drugs have anticholinergic, antiadrenergic and quinidine-like effects that can produce further cardiac decompensation in heart failure. Antidepressants are generally well tolerated except when toxic levels occur or in the most extremely compromised cardiac patients. Monoamine oxidase inhibitors should be used only in highly reliable patients to avoid the acute hypertensive crises that are well known to occur with these agents. Antipsychotic drugs with limited cardiovascular side effects can be used effectively and safely but care must be taken to avoid toxic levels which could produce excess hypotension or lethal arrhythmias. Lithium can also be used in heart failure if patients are effectively monitored to avoid toxic levels which could occur due to reduction in renal function, use of diuretics or imposition of a low sodium chloride diet. Evaluation and management of patients with mental symptoms and heart failure provides a strong challenge for the consulting psychiatrist.

Beta‐adrenoceptor responsiveness in hypertension: effects of dietary NaCl intake.

1. Adrenergic responsiveness may be an important determinant of peripheral resistance in man. We have demonstrated that vascular beta-adrenergic responsiveness is reduced in young borderline hypertensive subjects. A parallel defect in beta-adrenergic mediated adenylyl cyclase activity and beta-adrenoceptor affinity for agonists also has been identified in lymphocytes from borderline hypertensive subjects. In contrast, it is unclear whether cardiac beta-adrenergic responsiveness is altered. 2. The reduction in lymphocyte and vascular beta-adrenergic responsiveness is corrected when hypertensive subjects are fed a low sodium chloride diet. This pattern of regulation differs from that seen in young normotensive subjects fed a low NaCl diet where either reduced or unchanged beta-adrenergic responsiveness has been reported. 3. These studies suggest a generalized defect in beta 2-adrenergic responsiveness in borderline hypertensive subjects and demonstrate important differences between normotensive and hypertensive subjects in the pattern of beta-adrenoceptor regulation mediated by dietary sodium intake. The mechanism by which dietary sodium modulates beta-adrenergic responsiveness is yet to be determined.

Factors determining sodium chloride sensitivity of patients with essential hypertension

Factors which determine sodium chloride sensitivity, defined as the difference between the mean blood pressure after 1 week of a low sodium chloride diet (3 g/day) and that after 1 week of a high sodium chloride diet (20 g/day), were studied in 60 inpatients with essential hypertension using a multivariate analysis. The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. These data suggest that both intracellular sodium accumulation and inadequate suppression of the renin-angiotensin system may be independently involved in the elevation of blood pressure after sodium chloride loading. We could not find the independent importance of volume retention, hyperadrenergic activity or basal blood pressure in the sodium chloride sensitivity.

Role of cellular calcium in salt sensitivity of patients with essential hypertension.

The mechanism by which excessive sodium chloride intake raises blood pressure has not been fully clarified. The present study was therefore undertaken in patients with essential hypertension to investigate the possible role of an intracellular calcium-dependent mechanism in salt sensitivity. The difference in mean blood pressure between a week of low sodium chloride diet (3 g/day) and a week of high sodium chloride diet (20 g/day) was studied in relation to the intracellular free calcium concentration in lymphocytes and an acute hypotensive response to a 10-mg sublingual dose of nifedipine in 12 inpatients. Sodium chloride loading induced significant increases in mean blood pressure (from 111 +/- 12 to 122 +/- 11 mm Hg; p less than 0.01), intracellular free calcium in lymphocytes (from 133 +/- 13 to 145 +/- 9 nmol/L; p less than 0.01), and the hypotensive response to nifedipine (from 19 +/- 6 to 31 +/- 10 mm Hg; p less than 0.01). In addition, serum total calcium concentration was decreased while urinary calcium excretion was increased. The elevation of mean blood pressure was closely and positively correlated with the increase in intracellular free calcium concentration (r = 0.71, p less than 0.05) and the increase in the hypotensive effect of nifedipine (r = 0.91, p less than 0.01) after sodium chloride loading. However, changes in these values had no relation to the change in serum concentration or urinary excretion of calcium. These data suggest that change in the cellular calcium-dependent vasoconstriction mechanism may be associated with salt sensitivity of patients with essential hypertension.

Dietary Sodium Intake and Urinary Dopamine and Sodium Excretion During the Course of Blood Pressure Development in DAHL Salt-Sensitive and Salt-Resistant Rats

Recent studies have suggested that dopamine (DA) formed within the kidney may play an important role in promoting sodium excretion, and that renal production and excretion of DA is determined by dietary sodium intake. Inasmuch as increased sodium consumption produces hypertension in Dahl salt-sensitive (DS) rats but not in Dahl salt-resistant (DR) rats, the present study was designed to examine the relationship between sodium consumption and urinary excretion of DA in these rats. DS and DR rats were placed on either high sodium chloride (8%) or low sodium chloride (0.4%) diets at 4 weeks of age and their systolic blood pressure (SBP), urine volume, urinary sodium and catecholamine excretion were measured once every week for the next 4 weeks. High sodium chloride diet increased SBP in DS rats at 6 weeks of age and SBP continued to rise until they were 8 weeks old. The SBP of DR rats did not reach hypertensive levels when they were given high sodium chloride diet. The SBP of DS rats on low sodium chloride diet was significantly higher than DR rats on the same diet. The urinary DA excretion increased with age in all four groups of rats and was similar when they were 8 weeks old. However, both DS and DR rats on high sodium chloride diet excreted greater amounts of sodium and had increased urine volume compared to the DS and DR rats on low sodium chloride diet. There were no significant differences in urinary NE or E excretion in these four groups of rats. Kidney levels of DA and NE were significantly lower in DS compared to DR rats on high sodium chloride diet. These results show that although there are no differences in urinary DA excretion between rats on low and high sodium intake, both DS and DR rats on high sodium chloride diet are able to exhibit a natriuretic response. The DS rats eliminate sodium at the expense of an elevated SBP whereas DR rats stay normotensive. Therefore, it appears that alterations in mechanisms controlling renal vascular resistance rather than sodium excretion are responsible for the development of hypertension in DS rats.

Renal tubular acidosis in childhood

Renal tubular acidosis in childhood

Mineralocorticoid-resistant renal hyperkalemia without salt wasting (type II pseudohypoaldosteronism): Role of increased renal chloride reabsorption

A rare syndrome has been described in which mineralocorticoid-resistant hyperkalemia of renal origin occurs in the absence of glomerular insufficiency and renal sodium wasting and in which hyperchloremic acidosis, hypertension, and hyporeninemia coexist. The primary abnormality has been postulated to be a defect of the potassium secretory mechanism of the distal nephron. The present studies were carried out to investigate the mechanism of impaired renal potassium secretion in a patient with this syndrome. When dietary intake of sodium chloride was normal, renal clearance of potassium was subnormal (CK/GFR = 3.6 +/- 0.2%; normal subjects, 9.0 +/- 0.9%, N = 4) despite high normal or supernormal levels of plasma and urinary aldosterone. The fractional clearance of potassium remained subnormal (CK/GFR = 5.1 +/- 0.2%) during superimposed chronic administration of superphysiologic doses of mineralocorticoid hormone. Little increase in renal potassium clearance occurred when the delivery of sodium to distal nephron segments was increased further by the i.v. infusion of sodium chloride, despite experimentally sustained hypermineralocorticoidism. But potassium clearance increased greatly when delivery of sodium to the distal nephron was increased by infusion of nonchloride anions: sulfate (sodium sulfate infusion, low sodium chloride diet; CK/GFR = 63.7 +/- 0.4%) or bicarbonate (sodium bicarbonate plus acetazolamide infusion; CK/GFR = 81.7 +/- 1.7%). These findings indicate that mineralocorticoid-resistant renal hyperkalemia in this patient cannot be attributed to the absence of a renal potassium secretory capability or to diminished delivery of sodium to distal nephron segments; instead it may be dependent on chloride delivery to the distal nephron. We suggest that the primary abnormality in this syndrome increases the reabsorptive avidity of the distal nephron for chloride, which (1) limits the sodium and mineralocorticoid-dependent voltage driving force for potassium and hydrogen ion secretion, resulting in hyperkalemia and acidosis and (2) augments distal sodium chloride reabsorption resulting in hyperchloremia, volume expansion, hyporeninemia, and hypertension.

Electrolyte and water exchange in bronchial asthma, with emphasis on the influence of pitressin

In a previous communication, the authors have presented evidence which indicated that various procedures inducing electrolyte and water changes in the body had a definite influence upon persistent bronchial asthma. An extremely low sodium chloride diet improved the asthmatic conditions, and fever therapy then led to remissions. The remissions were terminated by the ingestion of sodium chloride. During the periods of increased salt intake, the subject drank more water, stored much of it, and gained weight. The question therefore arose as to whether the increased water storage or the extra salt was instrumental in precipitating the asthmatic symptoms. The action of the pressor principle of the posterior lobe of the pituitary gland offers an answer to this question. This hormone, pitressin, when injected subcutaneously, causes a retention of body fluids without the aid of an increase in body salts. Many asthmatic children were given pitressin, and six of them with intractable asthma who tolerated the hormone were subjected to special studies. A total of twenty observations were made; three of the most typical studies are presented graphically on a chart. The subjects were all placed on an extremely low sodium chloride diet, and when pitressin was administered, there was a retention of water up to 2 kg. in some of the patients. Improvement in the asthma began during the antidiuretic phase and continued through the diuretic and subsequent periods, proving that the storage of large amounts of water in the body and its sudden loss had apparently little influence on the asthmatic symptoms. A review of the literature discloses investigations which indicate that, during pitressin antidiuresis and diuresis, despite low salt intake, sodium chloride is excreted, leading to a marked loss of body salt. It is apparent that bronchial asthma can be ameliorated, even in the presence of excessive hydration, if there is an associated depletion of sodium chloride. No positive therapeutic implications are warranted at this time, since the procedures outlined in this communication may still be considered rather involved and technically difficult to carry out with effective exactness. The whole subject is, therefore, of value more as an investigative tool rather than a therapeutic procedure.