Sodium Concentration Of Saliva Research Articles

Diagnosing cystic fibrosis by elevated sodium concentration in saliva

Diagnosing cystic fibrosis by elevated sodium concentration in saliva

In vivo sodium release related to salty perception during eating model cheeses of different textures

The objective of this study was to determine to what extent the ratio of fat/water, fat/protein or water/protein concentrations and texture may influence the release of sodium, saltiness perception and chewing behaviour during eating food. Cheese models were manufactured with two levels of shear intensity and two different ratios of fat/water concentration. Sodium concentration in saliva, saltiness perception and masticatory parameters were evaluated for each subject and each product. The products made with high shear intensity released sodium more easily in the mouth during chewing, whilst high fat concentration contributed to reduce the release of sodium. Saltiness was only related to matrix composition (fat/water concentrations). Moreover, sodium release and saltiness perception were found to be correlated with several masticatory parameters. A model built with matrix composition variables showed that the water content influenced the sodium release and the fat content influenced saltiness, but with temporal differences during the chewing process.

Sodium concentration in saliva along the time course of experimental Coriolis sickness.

Procedures designed to evaluate the severity of motion sickness have included subjective reporting of changes in salivation. In order to increase objectivity, we studied the sodium concentration of saliva, which is directly related to the flow rate. Healthy adults with normal vestibular function underwent a modified Coriolis Sickness Susceptibility Index (CSSI) test, utilizing a staircase profile. Saliva was collected without interrupting the stimulus by means of cotton placed beneath the subject's tongue for one minute. Samples were obtained 5 min prior to stimulation, 30 and 45 min following stimulus onset, and/or upon reaching the "nausea II" endpoint. Saliva for analysis by atomic absorption spectrophotometry was obtained by centrifugation of the cotton. A significant difference in sodium concentration was found between the baseline and 30-min sample (p less than 0.01). Although the amount of salivation was rather variable, the pattern of changes in sodium concentration was similar in all experimental cases.

Sodium appetite: Species and strain differences and role of renin-angiotensin-aldosterone system

The characteristics of the appetite for NaCl in humans differ in some aspects from those in other species. The mechanisms of appetite for NaCl have been studied in detail in two species, rats and sheep. We review the treatments known to induce an appetite for NaCl in rats, with special reference to differences among strains in their spontaneous preference for NaCl solution. The current view of the mechanism is critically appraised, with particular emphasis on the role of angiotensin II, mineralocorticoids, cerebroventricular sodium transport, and the relation between preference for NaCl and the concentration of sodium in saliva. The appetite for NaCl in rodents other than rats is considered next, and reveals that mice, hamsters and gerbils are reluctant to ingest NaCl either spontaneously or after treatment with several of the natriorexigenic stimuli that are effective in rats. The characteristics of the appetite for NaCl in non-rodent species, including sheep, rabbit, dog, and non-human primates, are then described. We discuss some of the possible differences in mechanism that might account for this behavioral diversity among species.

Role of renin-angiotensin-aldosterone system in NaCl appetite of rats.

A variety of experimental paradigms is now known to induce an appetite for NaCl solutions in rats. These include 1) bilateral adrenalectomy; 2) hypothyroidism; 3) salivariectomy; and 4) administration of hydrochlorothiazide, metyrapone, estrogen, methylxanthines, captopril, propranolol, large doses of deoxycorticosterone acetate, and intraperitoneal isotonic glucose or subcutaneous polyethylene glycol. A point of commonality among these is that a reduction in preference threshold accompanies the appetite for NaCl in all cases thus far tested. An additional point is the fact that each paradigm inducing a salt appetite, except salivariectomy, can be linked to an effect on the renin-angiotensin-aldosterone system. The level of angiotensin II in the brain may play a role in the induction of a salt appetite in the rat. It is clear, however, that modest doses of mineralocorticoid hormones, given in conjunction with the stimulus producing the salt appetite (e.g., adrenalectomy, thyroidectomy, or treatment with captopril), reduces NaCl intake to control level. Although this effect can be partially explained in most cases by the consequent reduction in angiotensin II production, the salt appetite that occurs when mineralocorticoid concentration in blood is high and angiotensin II concentration is low, or when both are low, requires another explanation. This may be related to the effect of mineralocorticoid hormones on salivary sodium concentration. The role of the concentration of sodium in saliva on intake of NaCl solution provides an alternative explanation for the induction of a salt appetite in rats and merits additional study.

Statistical ritual in clinical journals: is there a cure?--I.

The shambles mentioned at the beginning of Part I referred to the confusion in the use of standard deviations and standard errors of means,1 with the latter apparently more popular, perhaps because they are so much smaller than their parent standard deviations and thus suggest higher precision. The author denned the standard deviation as representing the variation among the individual measurements,2 but this does not help us unless we know what multiple of standard deviation would enclose a certain percentage of the observations. The formula commonly used is mean ?1-96 SD (or 2 SD), on the assumption that we have individual measurements that, if increased in number, would form approximately a Gaussian distribution?an assumption for which most medical data provide scanty evidence. Bell shaped is not synonymous with Gaussian; and a trick such as the logarithmic transformation cannot be guaranteed to make the approximation safe. We should remember that the Gaussian curve started as the curve of error, a mathematical invention that was believed to represent the scatter of the variable (chance) errors in physical measurements, but thorough investigation3 failed to substantiate the belief. Perhaps, however, some authors producing a standard deviation do not visualise any distribution. If they did, I would expect to see comments when mean minus 2 SD (or even minus 1 SD) leads to a ridiculous negative value in data such as: sodium concentration in saliva before and after a certain drug treatment; days off work after minor surgery for haemorrhoids ; activity of an enzyme in ascitic fluid in hepatic cirrhosis; serum concentration of amyloid in rheumatoid arthritis; duration of labour; number of vaginal examinations during labour. The widespread use of the Gaussian distribution to express inter subject variation has been apparently due, firstly, to the illegitimate application of the mathematical term normal (Gaussian) as if synonymous with healthy,4 5 and, secondly, to the use of standard deviation to produce standard error of the mean in the Gaussian based t test.

Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption.

If high sodium intake is involved in the pathogenesis of essential hypertension, the effects of changing the sodium intake should be demonstrable in the susceptible part of the normotensive population. Therefore, we have investigated the effects of moderate salt restriction in 52 young normotensive subjects with and without a family history of hypertension; 22 (42%) responded to moderate salt restriction (200 to 50 mmol/day) over 2 weeks, with a significant fall in blood pressure shown by continuous automatic blood pressure recordings. Accordingly, these subjects were classified as salt-sensitive, and the remainder as salt-resistant. Compared to salt-resistant subjects, salt-sensitive subjects showed a 2.5-fold higher incidence of a positive family history of hypertension (p less than 0.01), and a significantly higher blood pressure and lower salivary sodium concentration during the usual high sodium diet. Although there were no differences in Na,K-ATPase activity and in Na-K cotransport of erythrocytes, the pressor response to infused norepinephrine in salt-sensitive subjects was double that of salt-resistant subjects independent of the diet and this was linked to indirect evidence for enhanced proximal tubular sodium reabsorption. On the usual high sodium diet, 40% of the normal population may be salt-sensitive and prone to develop hypertension. Hypersensitivity to catecholamines (genetically determined?) may be the cause of salt sensitivity. A low sodium concentration in saliva deserves further study as a simple screening test to identify salt-sensitive subjects.

Effect of x-irradiation on Na and K secretion by human parotid gland.

Experiments were carried out on 12 subjects to study the secretion of Na and K in the parotid saliva over secretory rates ranging from 0.06 to 2.2 ml/min. The possible effect of X-irradiation per se on such secretions was evaluated. Sodium concentration in saliva was linearly related to flow rate, whereas the potassium concentration was negatively correlated to salivary secretory rate. X-irradiation by itself did not influence the secretion of Na apart from its influence on flow rate. In the case of potassium, a significantly greater regression coefficient of potassium secretion per minute and flow rate was noted. This was associated with a significantly higher K/Na ratio in the saliva. Submitted on November 13, 1961

A Study of Sweat Electrolyte Excretion in A Patient Suffering from Congestive Heart Failure

Under normal circumstances the kidney regulates the body sodium content by balancing the output against the intake. In congestive heart diseases this regulation fails, the patient puts on weight and develops edema, and sodium nearly disappears from the urine. It has been maintained that not only the kidneys, but also other organs suppress the excretion of sodium in congestive heart failure. White, Gordon & Leiter( 1950) and Berger & Steele (1952) demonstrated a lowered sodium concentration in saliva, and Berger & Steele further demonstrated suppression of sodium excretion by the colon of edematous patients, and a lowered sodium concentration in the sweat. In two patients accumulating edema fluid the sweat sodium concentration was 8 and 13 mEq/l respectively, against an average of 39 mEq in normal individuals. Berger & Steele maintain that the accumulation of edema is due to a suppressed excretion of sodium through th? kidneys, the sweat and salivary glands, and the colon. In their opinion this retention iq due to an excess of a desoxycorticosteronelike hormone, capable of suppressing the excretion of sodium through various organs. Robinson & Robinson (1954), however, seriously doubt the correctness of Berger & Steele's explanation and suggest that the lowered sodium excretion through the skin may be an adaptation to salt depletion caused by carboxylic resin therapy. We have had the opportunity to study the excretion of electrolytes through the sweat in a case oi congestive heart failure. In this patient no peripheral edema appeared in spite of a very low renal sodium excretion. Our study revealed that this was due to a very heavy sweating which contained all the dietary sodium. The purpose of this paper is to report the results of the study.