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PubMed2001

Manipulating cattle distribution with salt and water in large arid-land pastures: a GPS/GIS assessment.

Several of the problems associated with grazing animals in extensive settings are related to their uneven patterns of use across the landscape. After fencing, water and salt are two of the most frequently used tools for affecting cattle distribution in extensive settings. Cattle are attracted to water in arid regions, but mixed results have been obtained with salt and mineral supplements. The goal of this study was to evaluate the efficacies of salt and water manipulations for affecting cattle distribution in large (>825ha) pastures. This was accomplished by fitting cattle with global positioning system (GPS) collars and monitoring their travels and activities in a three pasture, Latin-square design where water and salt shared a common location and water or salt were moved individually to distant areas. Mean distance of cattle from water (&xmacr;=1.16km) was unaffected by treatments (P=0.79) suggesting that cattle followed movements of water tanks. Distance traveled daily (&xmacr;=5.78km), time devoted to grazing (11.0h per day), time devoted to resting (10.1h per day), and the area (&xmacr;=325ha) of minimum convex polygons were also unaffected by treatment implying that cattle did not compensate for separated water and salting areas with increased travels or disruptions of habitual grazing and resting activities. Centers of activity for cattle shifted further (P=0.02) when water (&xmacr;=1.49km) was moved than when salt (&xmacr;=1.00km) was relocated. Mean distance of cattle from salt increased from 1.03km, when salt and water were together, to 1.73km (P=0.08) when salt and water were separated. This implied that cattle made less effort to remain near salt. Also, when water and salt were separated, cattle were found within 250m of water 354 times and close to salt only 38 times. Movement of drinking water to distant points in pastures was the most effective tool for altering cattle distribution. When cattle and salt were introduced to a new portion of a pasture, cattle used the new area for about 2 days, and then began drifting back toward previously used portions of the pasture. Manipulations of salting stations will not significantly rectify serious livestock distribution problems in extensive arid-land pastures.

Journal Article↗
PubMed2003

No evidence of a relation between 11beta-hydroxysteroid dehydrogenase type 2 activity and salt sensitivity.

BACKGROUND: The ratio of urinary concentrations of tetrahydrocortisol plus allotetrahydrocortisol to tetrahydrocortisone [(THF + ATHF)/THE] reflects the activity of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11BHSD2), which converts cortisol to cortisone in the kidney and thereby protects the mineralocorticoid receptor from the mineralocorticoid action of cortisol. The aim of the present study was to investigate whether 11BHSD2 activity is affected by salt intake and if it is related to salt sensitivity. METHODS: Concentrations of THF, ATHF, and THE in 24-h urine collections was determined by gas chromatography at baseline, after 1 week on a low salt diet (10 mmol/d), and after another week on a high salt diet (240 mmol/d) in 29 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure (BP) after the high salt diet and mean arterial BP after the low salt diet. RESULTS: The high salt diet increased (THF + ATHF)/THE by 5.1% +/- 9.4% (P =.009) when compared to the low salt diet. The salt-induced change of (THF + ATHF)/THE was not related to salt sensitivity. There was no correlation between salt sensitivity and (THF + ATHF)/THE at baseline (r = -0.18, P =.34), whereas salt sensitivity was inversely related to (THF + ATHF)/THE after the low (r = -0.38, P =.05) and after the high (r = -0.39, P =.04) salt diets. CONCLUSIONS: We found no support for an association between enhanced salt sensitivity and reduced 11BHSD2 activity.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1997

Chronic salt overload increases blood pressure and improves glucose metabolism without changing insulin sensitivity.

The effect of sodium chloride salt restriction and overload on insulin sensitivity is still an open question. Some authors have shown that NaCl salt restriction increases insulin resistance, whereas others have reported the opposite. In the present study, the objective was to get some more insight on this issue by studying the influence of dietary salt content on glucose uptake in isolated adipocytes. Male Wistar rats were fed from weaning either low (0.15%) or high (7.94%) salt diets. On the 12th week of age, weight and tail-cuff blood pressure were measured, followed 10 days later by an intravenous glucose tolerance test with concomitant insulin determinations. One week later, the rats were killed by decapitation and epididymal adipocytes were obtained for glucose metabolism evaluation. No weight differences were observed between both groups of animals. Blood pressure was significantly higher (P < .001) on salt overloaded rats (146 +/- 11 mm Hg) than on salt restricted ones (115 +/- 5 mm Hg). Dietary salt content did not influence the area under the curve of plasma glucose. Area under the curve of insulin levels was lower (P = .023) on the high than on the low salt diet. A higher (P < .001) glucose uptake in the absence and in the presence of insulin was observed in adipocytes from rats on the high salt diet. The median effective concentration (EC50) from the dose-response curves of glucose uptake was the same on both groups of animals. Glucose oxidation and incorporation into lipids was also enhanced by salt overload. High salt increased insulin receptor density (P < .001). In conclusion, salt overload increased blood pressure, and high and low salt dietary content did not influence insulin sensitivity based on the unchanged EC50 from the in vitro studies. However, insulin-independent glucose uptake, oxidation, and incorporation into lipids were enhanced in adipocytes from rats on the high salt diet. The lower levels of insulin during the glucose tolerance test on salt-loaded animals may be a consequence of the higher insulin-independent glucose uptake in that group.

Adipocytes↗
PubMed2001

Increased insulin resistance in salt sensitive essential hypertension.

OBJECTIVE: To determine the possible relationship between insulin resistance and salt sensitivity in essential hypertension. DESIGN AND METHODS: We studied 17 non-obese, essential hypertensive patients (24-h blood pressure: 149 +/- 15/94 +/- 5 mm Hg) with normal glucose tolerance. Salt sensitivity was diagnosed in the presence of a significant increase (P < 0.05, more than 4 mm Hg) in 24-h mean blood pressure (MBP) when patients switched from a low-salt intake (50 mmol/day of Na(+)) to a high-salt intake (240 mmol/day of Na(+)), each period lasting 7 days. The insulin sensitivity index was determined by the euglycaemic hyperinsulinaemic clamp. RESULTS: Six patients were classified as salt sensitive (24-h MBP increase: 6.2 +/- 1.1 mm Hg), and 11 as salt resistant (24-h MBP increase: -1.2 +/- 3.8 mm Hg). No significant differences were observed between salt sensitive and salt resistant patients regarding baseline characteristics, fasting serum insulin, fasting serum glucose, glycosylated haemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, uric acid and microalbuminuria. Salt sensitive patients exhibited a reduced insulin sensitivity index compared with salt resistant patients (1.7 +/- 1.1 vs 3.5 +/- 1.2 mg/kg/min; P = 0.009). An inverse relationship (r -0.57; P = 0.016) between the insulin sensitivity index and 24-h MBP increase with high salt intake was found. CONCLUSION: Salt sensitive essential hypertensive patients are more insulin resistant than salt resistant patients when both salt sensitivity and insulin resistance are accurately measured. Indirect measures of both insulin and salt sensitivity and/or the presence of modifying factors, such as obesity or glucose intolerance, may account for differences in previous studies.

Adult↗
PubMed2002

Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health.

Two recent meta-analyses of randomised salt reduction trials have concluded that there is little purpose in reducing salt intake in the general population. However, the authors, as with other previous meta-analyses, included trials of very short duration (eg 1 week or less) and trials of acute salt loading followed by abrupt reductions to very low salt intake (eg from 20 to less than 1 g of salt/day). These acute salt loading and salt depletion experiments are known to increase sympathetic tone, and with salt depletion cause a rise in renin release and, thereby, plasma angiotensin II. These trials are not appropriate, therefore, for helping to inform public health policy, which is for a more modest reduction in salt intake, ie, from a usual intake of approximately 10 to approximately 5 g of salt per day over a more prolonged period of time. We carried out a meta-analysis to assess the effect of a modest salt reduction on blood pressure. Our data sources were MEDLINE, EMBASE, Cochrane library, CINAHL, and the reference lists of original and review articles. We included randomised trials with a modest reduction in salt intake and a duration of 4 or more weeks. Meta-analysis, meta-regression, and funnel plots were performed. A total of 17 trials in hypertensives (n=734) and 11 trials in normotensives (n=2220) were included in our study. The median reduction in 24-h urinary sodium excretion was 78 mmol (equivalent to 4.6 g of salt/day) in hypertensives and 74 mmol in normotensives. The pooled estimates of blood pressure fall were 4.96/2.73+/-0.40/0.24 mmHg in hypertensives (P<0.001 for both systolic and diastolic) and 2.03/0.97+/-0.27/0.21 mmHg in normotensives (P<0.001 for both systolic and diastolic). Weighted linear regression analyses showed a dose response between the change in urinary sodium and blood pressure. A reduction of 100 mmol/day (6 g of salt) in salt intake predicted a fall in blood pressure of 7.11/3.88 mmHg (P<0.001 for both systolic and diastolic) in hypertensives and 3.57/1.66 mmHg in normotensive individuals (systolic: P<0.001; diastolic: P<0.05). Our results demonstrate that a modest reduction in salt intake for a duration of 4 or more weeks does have a significant and, from a population viewpoint, important effect on blood pressure in both hypertensive and normotensive individuals. This meta-analysis strongly supports other evidence for a modest and long-term reduction in population salt intake, and would be predicted to reduce stroke deaths immediately by approximately 14% and coronary deaths by approximately 9% in hypertensives, and reduce stroke and coronary deaths by approximately 6 and approximately 4%, in normotensives, respectively.

Blood Pressure↗
PubMed1984

Solution structure of poly(dA-dT).poly(dA-dT) in low and high salt: a 500 MHz 1H NMR study using one-dimensional NOE.

CD spectra of poly(dA-dT).poly(dA-dT) in low salt (10-100 mM NaCl) and high salt (4-6 M CsF) are different i.e. 275 nm band gets inverted in going from low to high salt (Vorhickova et. al., J. Mol. Biol. 166, 85, 1983). However, from CD spectra alone it is not possible to decipher any structural differences that might exist between the low and high salt forms of poly(dA-dT).poly(dA-dT). Hence, we took recourse to high resolution NMR spectroscopy to understand the structural properties of poly(dA-dT).poly(dA-dT) in low and high salt. A detailed analysis of shielding constants and extensive use of NOE studies under minimum spin diffusion conditions using C(8)-deuterated poly(dA-dT).poly(dA-dT) enabled us to come up with the following conclusions (i) base-pairing is Watson-Crick under low and high salt conditions. (ii) under both the conditions of salt the experimental data can be explained in terms of an equilibrium blend of right and left-handed B-DNA duplexes with the left-handed form 70% and the right-handed 30%. In a 400 base pairs long poly(dA-dT).poly(dA-dT) (as used in this study), equilibrium between right and left-handed helices can also mean the existence of both helical domains in the same molecule with fast interchange between these domains or/and unhindered motion/propagation of these domains along the helix axis. (iii) However, there are other structural differences between the low and high salt forms of poly(dA-dT).poly(dA-dT); under the low salt condition, right- and left-handed B-DNA duplexes have mononucleotide as a structural repeat while under the high salt conditions, right- and left-handed B-DNA duplexes have dinucleotide as a structural repeat. In the text we provide the listing of torsion angles for the low and high salt structural forms. (iv) Salt (CsF) induced structural transition in poly(dA-dT).poly(dA-dT) occurs without any breakage of Watson-Crick pairing. (v) The high salt form of poly(dA-dT).poly(dA-dT) is not the left-handed Z-helix. Although the results above from NMR data are quite unambiguous, a question still remains i.e. what does the salt (CsF) induced change in the CD spectra of poly(dA-dT).poly(dA-dT) really indicate? Interestingly, we could show that the salt (CsF) induced change in poly(dA-dT).poly(dA-dT) is quite similar to that caused by a basic polypeptide viz. poly-L(Lys2-Ala)n i.e. both the agents induced a psi-structure in DNA.

Cesium↗
PubMed1991

Salt sensitivity in young normotensive subjects is associated with a hyperinsulinemic response to oral glucose.

Insulin resistance associated with a hyperinsulinemic response to oral glucose intake has been found in patients with essential hypertension and is believed to play a role in inducing hypertension by causing renal sodium and water retention. We therefore examined whether salt-sensitive, young normotensives, assumed to be predisposed to essential hypertension, exhibit impaired glucose tolerance in a similar way. The plasma insulin and glucose response to oral glucose intake (75 g) was assessed in 23 healthy, lean, male volunteers ingesting either 20 mmol or 260 mmol NaCl/day for 6 days each in a single-blind randomized crossover study. Salt sensitivity was defined as a significant drop in mean arterial blood pressure greater than 3 mmHg (means of 30 readings in the supine subject; P less than 0.05) under the low-salt diet. Following the glucose load, plasma levels of both glucose and insulin were significantly higher (P less than 0.01) in the salt-sensitive (n = 10) compared with the salt-resistant subjects (n = 13) during the high-salt diet but not during the low-salt diet. Whereas in the salt-sensitive group glucose tolerance improved with dietary salt restriction (P less than 0.01), it deteriorated in the salt-resistant group (P less than 0.05). Following the glucose load under the high-salt diet, there was a significant drop in blood pressure in the salt-sensitive (P less than 0.005) but not the salt-resistant subjects. The hyperglycemic and hyperinsulinemic response in salt-sensitive subjects suggests that insulin resistance is present in these subjects prior to the development of hypertension and that it can be ameliorated by salt restriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Overexpression of chloride channel CLC-K2 mRNA in the renal medulla of Dahl salt-sensitive rats.

OBJECTIVE: The present study aimed to characterize the influence of salt intake on the gene expression of the kidney specific chloride channels CLC-K1 and CLC-K2 in the kidneys of salt-resistant and salt-sensitive Dahl rats. DESIGN: For this purpose Dahl salt-resistant (Dahl-R) and Dahl salt-sensitive rats (Dahl-S) were fed a low (0.02%), normal (0.6%) or high (4%) salt diet for 19 days and CLC-K1 and -K2 mRNA expression was semiquantitated in cortex, outer and inner medulla. METHODS: Kidneys were macroscopically dissected, total RNA was isolated according to the guanidinium-thiocyanate-phenol-chloroform method and messenger RNAs for the kidney specific chloride channels CLC-K1 and CLC-K2 were measured by ribonuclease protection assay. RESULTS: Systolic blood pressure in high salt-treated Dahl-S rats increased to 204 +/- 5 mmHg versus 150 +/- 7 mmHg in Dahl-S controls. Dahl R and low salt Dahl-S rats showed no increase in blood pressure. For CLC-K1 mRNA we found an order of abundance inner medulla >> outer medulla >> cortex. There was no difference in mRNA abundance between Dahl-R and -S, nor any effect of the rate of salt intake on CLC-K1 mRNA abundance in the different kidney zones. CLC-K2 mRNA expression in cortex and outer medulla was similar between Dahl-R and -S rats. In the inner medulla, however, CLC-K2 mRNA was 1.7-fold higher in Dahl-S than in Dahl-R rats. In the cortex we found no influence of salt intake on CLC-K2 mRNA. In outer and inner medulla of Dahl-R rats and Dahl-S rats high salt diet led to a marked downregulation of CLC-K2 mRNA expression. Consequently, CLC-K2 gene expression in the inner medulla was 2.2-fold higher in Dahl-S than in Dahl-R rats in states of high salt diet. CONCLUSION: Given that the CLC-K2 chloride channel in the outer and inner medulla contributes to salt reabsorption, our findings would suggest that Dahl-S rats have an increased medullary salt reabsorption. This may contribute to the inability of these animals to excrete an increased salt load at a normal renal perfusion pressure leading to the development of hypertension.

Animals↗
PubMed2005

Increased salt appetite in patients with congenital adrenal hyperplasia 21-hydroxylase deficiency.

Salt appetite was investigated in 14 patients with congenital adrenal hyperplasia of the salt-wasting form (SW group), 12 patients with the simple virilized form who are not salt losing, and 18 healthy siblings. Salt appetite was evaluated by questionnaire, preference tests, and dietary analyses. The findings showed that SW who were not therapeutically normalized showed increased salt appetite but no change in sweet preference. Their salt appetite correlated with symptoms of salt wasting, namely, plasma renin activity, plasma K(+), and urine Na(+) and (inversely) with blood pressure. Sensitivity to the taste of NaCl was not altered. Factor analyses of a larger group confirmed the distinction between salt appetite and sweet preference, but intake of dietary Na(+) and sweet carbohydrates and intake of salty and sweet snacks did not reflect distinct salt or sweet preferences. We confirm that putative perinatal dehydration, due to maternal nausea and vomiting during pregnancy, childhood vomiting, and diarrhea with occasional saline infusion, was related to increased salt appetite in adolescence. The findings suggest that salt appetite in humans is determined by interdependent, innate, physiological, and acquired attributes. Salt appetite in SW patients is an adaptive response mediated by the renin-angiotensin system, an innate predisposition to acquire salt preference (in anticipation of both sodium loss and its consequence), and imprinting by perinatal hyponatremic occurrences. Our findings contribute to understanding human salt intake, provide insight into the motivation for salt in patients with congenital adrenal hyperplasia 21-OH deficiency, and may point the way to improvements in therapeutic compliance in these patients.

Adolescent↗
PubMed1997

Salt loading enhances rat renal TxA2/PGH2 receptor expression and TGF response to U-46,619.

The tubuloglomerular feedback (TGF) response is potentiated by thromboxane A2 (TxA2) and/or prostaglandin endoperoxide (PGH2) acting on specific receptors. Infusion of the TxA2/PGH2 mimetic, U-46,619, into conscious rats leads to hypertension that is potentiated by a high-salt intake. Therefore, we tested the hypothesis that a high-salt intake enhances the expression of transcripts for TxA2/PGH2 receptors in the kidney and glomeruli and enhances the response of TGF to TxA2/PGH2 receptor stimulation. Groups of rats were accommodated to a low-salt (LS), normal salt (NS), or high-salt (HS) diet for 8-10 days. TxA2/PGH2 receptor mRNA was detected by reverse transcription-polymerase chain reaction in kidney cortex, isolated glomeruli, and abdominal aorta. TxA2/PGH2 mRNA abundance was significantly (P < 0.001) increased during intake of high-salt compared with low-salt diets in the kidney cortex (1.34 +/- 0.10 vs. 0.84 +/- 0.04 arbitrary units) and isolated outer cortical glomeruli (0.68 +/- 0.04 vs. 0.32 +/- 0.03 arbitrary units), but there was no effect of salt on TxA2/PGH2 receptor mRNA expression in the aorta. Maximal TGF responses were assessed from the increase in proximal stop flow pressure (an index of glomerular capillary pressure) during increases in loop of Henle perfusion with artificial tubular fluid from 0 to 40 nl/min. Compared with vehicle, the enhancement of maximal TGF with U-46,619 (10(-6) M) added to the perfusate was greater in rats adapted to high-salt than normal salt (HS: +9.6 +/- 1.1 vs. NS: +5.1 +/- 0.4 mmHg; P < 0.001) or low-salt (LS: +3.8 +/- 1.3 mmHg; P < 0.001) intakes. Responses to U-46,619 at each level of salt intake were blocked by > 70% by the TxA2/PGH2 receptor antagonist ifetroban. In contrast, enhancement of TGF by peritubular capillary perfusion of arginine vasopressin (AVP; 10(-7) M) was similar in high-salt and low-salt rats (HS: +1.5 +/- 0.6 vs. LS: +1.6 +/- 0.5 mmHg; not significant). We conclude that salt loading increases selectively the abundance of TxA2/PGH2 receptor transcripts in the kidney cortex and glomerulus, relative to the aorta, and enhances selectively TGF responses to TxA2/PGH2 receptor activation but not to AVP.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

Analbuminemic Nagase rats: blood pressure response to dietary salt challenge.

BACKGROUND: The role of albumin on blood pressure response to different salt challenges is not known. Therefore, we studied the blood pressure response of analbuminemic Nagase rats (NAR) to different salt challenges. 11beta-Hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the enzyme regulating the glucocorticoid access to the mineralocorticoid receptor, an enzyme that is decreased in humans with salt sensitive hypertension and other diseases with abnormal renal salt retention, was assessed during salt challenges. METHODS: Blood pressure was measured continuously by an intra-arterial catheter and a telemetry system in NAR (n = 8). NAR were set successively for 7 days on a normal (0.45% NaCl), high (8% NaCl), low (0.1% NaCl) and normal salt diet again, to assess salt related response in mean systolic (SBP) and diastolic blood pressure (DBP). 11beta-HSD2activity was assessed by measuring the urinary (THB + 5alpha-THB)/THA ratio with gas chromatography - mass spectrometry. RESULTS: Mean SBP and DBP increased with high salt intake (normal salt vs. high salt: SBP: 114 +/- 1 vs.119 +/- 3 mm Hg, p < 0.01; DBP: 84 +/- 1 vs. 88 +/- 3 mm Hg; n = 8; p < 0.01). Urinary (THB +5alpha-THB)/THA ratio increased during the high-salt period when compared to the normal-salt period (high salt vs. normal salt: 0.52 +/- 0.10 vs. 0.37 +/- 0.07; p = 0.05) indicating decreased 11beta-HSD2activity. CONCLUSION: Analbuminemic Nagase rats express increased blood pressure and reduced 11beta-HSD2 activity in response to a high-salt diet.

Adaptation, Physiological↗
PubMed1991

High salt intake. Sensory and behavioral factors.

Salt (NaCl) is a ubiquitous component of diets in developed countries. A major reason for this is that people judge many salted foods as more palatable than the same foods without salt. Because recent evidence indicates that an acceptable salt substitute is unlikely, an understanding of the behavioral and sensory factors involved in maintaining high salt preference is a prerequisite to successful programs aimed at reducing intake. Although little evidence exists for a genetic determination of individual differences in consumption and preferred level of salt, more research in this area is necessary. Considerable data support the view that the optimal level of salt in the diet is determined in part by the level an individual is currently consuming; increasing or decreasing customary salt intake, as long as the salt is tasted, increases or decreases the preferred level of salt in food. Although these data are consistent with a hypothesis that optimal salt preferences are learned, other data, from both animal models and human developmental studies, suggest that salt preference has an innate component. Furthermore, early experience with low or high salt diets may have a long-term impact on preferred salt levels. Liking for salt, similar to liking for sweets, has an innate basis that can be modified by individual experience.

Behavior↗
PubMed1992

Salt supplementation does not alter the pressor effect of blocking atrial natriuretic peptide in nucleus tractus solitarii.

We have previously shown that microinjection of monoclonal antibody to atrial natriuretic peptide (ANP) into the caudal nucleus tractus solitarii causes a pressor response in salt-sensitive spontaneously hypertensive rats (SHR) fed a basal (1%) salt diet, suggesting that endogenous ANP in this region may be involved in the centrally mediated regulation of blood pressure in this model. The present study tested the hypothesis that the pressor effect of blocking endogenous ANP in caudal nucleus tractus solitarii is enhanced by dietary salt supplementation in salt-sensitive SHR. Monoclonal antibody to ANP (0.55 micrograms) in 50 nl artificial cerebrospinal fluid or control immunoglobulin G was microinjected into the caudal nucleus tractus solitarii of conscious salt-sensitive SHR, salt-resistant SHR, and Wistar-Kyoto rats fed 1% or 8% salt diets for 3 weeks. Microinjection of the monoclonal antibody into the caudal nucleus tractus solitarii evoked similar increases in mean arterial pressure in salt-sensitive SHR on both 1% and 8% salt diets and in salt-resistant SHR on a 1% salt diet but had no effect in Wistar-Kyoto rats. In contrast, microinjection of control immunoglobulin G into this brain area did not alter mean arterial pressure or heart rate in any experimental group. Thus, endogenous ANP in caudal nucleus tractus solitarii mediates tonic control of blood pressure in both salt-sensitive and salt-resistant SHR but not in Wistar-Kyoto rats, and this effect is independent of the salt sensitivity of hypertension and of dietary salt intake.

Animals↗
PubMed1993

Renal acid-base excretion in normotensive salt-sensitive humans.

Reduced extracellular pH and bicarbonate levels recently have been reported in normotensive salt-sensitive subjects. To assess the possible role of altered renal acid-base handling in the perturbation of acid-base status in these individuals, we measured the renal acid-base excretion after an acute oral administration of either an alkali or acid load in normotensive salt-sensitive and salt-resistant men. Twenty-four young (22 to 29 years old), healthy male volunteers were placed on a low-salt diet (20 mmol NaCl per day) for 2 weeks with either 220 mmol NaCl or placebo added to the low-salt diet for 1 week each in a randomized single-blind crossover order. Salt sensitivity was defined as a significant drop in mean arterial pressure (> 3 mm Hg, mean of 60 readings taken on the seventh day of each diet, P < .05) during the low-salt diet. On the fifth and seventh days of each week, subjects were given an oral load of either sodium citrate (0.7 mmol/kg) or ammonium chloride (2.2 mmol/kg), respectively, in a randomized order, and arterial and urinary acid-base status was assessed at baseline and followed for 8 hours thereafter. According to the above definition, 13 subjects were considered salt sensitive. During the high-salt diet, mean arterial pressure was higher in the salt-sensitive than in the salt-resistant group (P < .01). Cumulative urinary bicarbonate excretion after the administration of sodium citrate was lower in the salt-sensitive than in the salt-resistant subjects during both the low-salt (46%, P < .001) and high-salt (32%, P < .01) diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1994

Microalbuminuria in salt-sensitive patients. A marker for renal and cardiovascular risk factors.

We previously showed that a high salt diet increases glomerular capillary pressure in salt-sensitive hypertensive patients and suggested that this may underlie the greater propensity of these patients to develop renal failure. Because microalbuminuria is considered an initial sign of renal damage, we have tested whether salt-sensitive patients display greater urinary albumin excretion than salt-resistant hypertensive patients. Twenty-two patients were placed on a low sodium intake (20 mEq/d) for 7 days followed by a high sodium diet (250 mEq/d) for 7 more days. Twelve patients were classified as salt sensitive and 10 as salt resistant. Urinary albumin excretion was greater in salt-sensitive than salt-resistant patients (54 +/- 11 versus 22 +/- 5 mg/24 h, P < .01). During the low sodium diet, glomerular filtration rate, renal plasma flow, and filtration fraction were similar between the two groups. During the high sodium intake, glomerular filtration, renal plasma flow, filtration fraction, and calculated intraglomerular pressure did not change in salt-resistant patients; in salt-sensitive patients, however, renal plasma flow decreased, and filtration fraction and intraglomerular pressure increased, whereas glomerular filtration rate did not change. Urinary albumin excretion was significantly correlated with glomerular capillary pressure. Salt-sensitive patients displayed higher serum levels of low-density lipoprotein cholesterol and lipoprotein(a) and lower levels of high-density lipoprotein cholesterol than salt-resistant patients. These studies have shown greater urinary albumin excretion and serum concentrations of atherogenic lipoproteins in salt-sensitive than in salt-resistant hypertensive patients, suggesting that salt sensitivity may be a marker for greater risk of renal and cardiovascular complications.

Albuminuria↗
PubMed1998

Inorganic indicators of the origin of edible salts marketed in Spain from a chemometric approach.

Twenty edible salts marketed in Spain were studied for content of inorganic constituents in order to identify one or more indicators of the origins of salts. In Spain the principal source of salt is seawater, either from the Mediterranean coast or from the Atlantic coast. In addition, some manufactured salts in the dietary category were also considered. Five "Atlantic," 12 "Mediterranean," and 3 dietary salts were analyzed for potassium, magnesium, calcium, strontium, manganese, zinc, and sulfate contents and for alkalinity. Salt samples were first dried for moisture determination. Metals were determined by inductively coupled plasma atomic emission spectrometry, sulfate was determined by turbidimetry, and alkalinity was determined by titration with hydrochloric acid. All the results were expressed as the means for triplicate experiments, as mg of analyte per kg of salt on a dry basis. From these results and by application of chemometric strategies (principal component analysis, variable-variable plots, and cluster analysis) it was found that the potassium content distinguishes sea salts from dietary salts very well, and the contents of strontium and manganese discriminate salts of Atlantic origin versus salts of Mediterranean origin. Dietary salts showed levels of potassium higher than the sea salts, and salts of Atlantic origin had greater strontium and manganese content values than salts of Mediterranean origin.

Potassium↗
PubMedDate not supplied

[Assessment of salt intake in hemodialysis].

One of the main goals of dialysis is to reach a correct sodium balance. Dietary sodium restriction facilitates control of thirst, water overload, hypertension and cardiac failure. Nowadays, it is possible to estimate sodium mass transfer and known interdialytic salt intake, by means of non-invasive methods. The use of dialysate sodium profiles improves dialysis tolerance but it has been reported that interdialytic thirst may increase because of an inappropriate sodium balance. The aim of this study was to evaluate the usual salt intake in hemodialysis patients, the effects on interdialytic gain weight, arterial pressure, blood volume preservation and dialysis tolerance of two different profiles of dialysate sodium and an additional session with salt restriction. Seventeen dialysis patients, 12 male and 5 females, were studied. Each patient underwent seven hemodialysis treatments: three consecutives sessions (a week) with constant sodium and ultrafiltration hemodialysis; three consecutive sessions with exponential decrease of conductivity (Initial 15.5-16.0, mid-session 14.3 and at the end 13.9-14 mS/cm) and ultrafiltration (1.6 l/h initial and 0.1 at the end) profiled hemodialysis; and an additional session which had a special dietary salt restriction. Dialysis parameters and dry weight were kept constant. Integra monitor with Diascan and Hemoscan biosensors (Hospal) were used in all sessions. We measured pre- and postdialytic plasma conductivity, sodium mass transfer, interdialytic weight gain, mean arterial pressure (MAP), percent reductions of blood volume (%R-BV) and hypotensive episodes during dialysis. Mean sodium mass transfer was 1,144 +/- 356 mmol (no profile week) vs 1,242 +/- 349 mmol (week with profiles), NS. It was equivalent to a salt ingestion of 9.6 +/- 3 and 10.4 +/- 3 g/day respectively. End plasma conductivity was 14.04 +/- 0.14 (no profile) versus 14.21 +/- 0.08 mS/cm (profiled), p < 0.001. Interdialytic weight gain was 2.49 +/- 0.76 (no profile) vs 2.32 +/- 0.56 kg (profiled), NS. MAP was 101 +/- 11 (no profile) vs 99 +/- 10 mmHg (profiled), NS. The %R-BV was -7.73 +/- 3 (no profile) vs -6.46 +/- 3% (profiled), p < 0.01. Hypotensive episodes/session were 0.66 +/- 0.75 (no profiles) vs 0.41 +/- 0.57 (profiled), NS. Mean sodium mass transfer was 356 +/- 125 mmol with usual salt intake and 240 +/- 81 mmol with salt restriction, p < 0.001. It was equivalent to a salt ingestion of 10.47 +/- 3 versus 7.06 +/- 2 g per day respectively, p < 0.001. Initial plasma conductivity was 14.31 +/- 0.21 (usually sodium intake) versus 14.16 +/- 0.17 mS/cm (salt restriction), p < 0.01. Predialysis blood pressures were decreased with dietary salt restriction, MAP was 99.1 +/- 11 vs 94.4 +/- 12 mmHg (p < 0.01). Interdialytic weight gain decreased with salt restriction, 2.32 +/- 0.76 vs 1.78 +/- 0.49 kg (p < 0.001). The %R-BV was -7.25 +/- 2 (usual sodium intake) vs -5.91 +/- 2% (salt restriction), p < 0.01. Hypotensive episodes/session were 0.71 +/- 0.8 (usual sodium intake) vs 0.18 +/- 0.5 (salt restriction), p < 0.05. In conclusion, automatic measurement of sodium mass transfer is a practical tool to follow dietary salt ingestion in hemodialysis patients. It allows us accurate, individualised and continual dietary interventions. The use of exponential decrease sodium profiles improve dialysis tolerance without changes in sodium balance, interdialytic weight gain or arterial pressure. A reduction of three g in salt intake observed in this study was beneficial in interdialytic weight gain, dialysis tolerance and blood pressure control.

Female↗
PubMed2001

Iodine concentration in household salt in South Africa.

OBJECTIVE: To determine the iodine concentration in household salt, the coverage of adequately iodized salt, the use of non-iodized agricultural and producers' salt, and the usefulness of salt as a carrier of iodine, and to relate these observations to socioeconomic status in South Africa. METHOD: The iodometric titration method was used to analyse 2043 household salt samples collected using a national, multistage, stratified, cluster survey. FINDINGS: The national mean and median iodine concentrations of household salt were 27 mg/kg (95% confidence interval (CI): 25-29 mg/kg) and 30 mg/kg (range = 0-155 mg/kg), respectively. There was considerable variation within and between geographical areas. Coverage of adequately iodized household salt, i.e. iodized at > 15 mg/kg, was 62.4% of households (95% CI: 58.8-66.0%) two years after the introduction of compulsory iodization at a level of 40-60 mg/kg. A total of 7.3% of households used non-iodized agricultural salt and salt obtained directly from producers. People at the lower end of the socioeconomic spectrum were more likely to suffer the consequences of using under-iodized salt because more of them used agricultural or coarse salt than did people in the higher socioeconomic categories. The iodine concentration in salt was lower in rural areas than in urban and periurban areas. CONCLUSIONS: The consequences of using under-iodized or non-iodized salt were most likely to be experienced in the country's three northern provinces, among people in the low socioeconomic categories, and in rural households. Since 95.4% of households in South Africa use salt regularly and 2.9% use it occasionally, the national iodization programme has the potential to meet the iodine requirements of the population. However, this can only be achieved if the primary reasons for the inadequate iodization of salt are eliminated and if special attention is given to vulnerable groups.

Cross-Sectional Studies↗