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At least 19 recordsLinked to original sources

PubMed1984

Mechanism of protein salting in and salting out by divalent cation salts: balance between hydration and salt binding.

The preferential interactions of proteins with solvent components were studied in concentrated aqueous solutions of the sulfate, acetate, and chloride salts of Mg2+, Ba2+, Ca2+, Mn2+ and Ni2+ [except for CaSO4, BaSO4, Mn-(OAc)2, and Ni(OAc)2], and results were compared with those of the Na+ salts. It was found that, for all the salts, the preferential hydration increased in the order of Cl- less than CH3-COO- less than SO42- regardless of the cationic species used, in agreement with the anionic lyotropic series, and that the same parameter exhibited a tendency to increase in the order of Mn2+, Ni2+ less than Ca2+, Ba2+ less than Mg2+ less than Na+. The salting-out and stabilizing or salting-in and destabilizing effectiveness of the salts were interpreted in terms of the observed preferential interactions. The surface tension increment of salts, which is a major factor responsible for the preferential interactions of the Na+ salts, had no correlation with those of the divalent cation salts. It was shown that the binding of divalent cations to the proteins overcomes the salt exclusion due to the surface tension increase, leading to a decrease in the preferential hydration. In conformity with this mechanism, the preferential interaction of MgCl2 was strongly pH dependent, because of the protein charge-dependent affinity of Mg2+ for proteins, while NaCl showed no pH dependence of the preferential interaction. The proposed mechanism was supported by a strong correlation between the preferential interaction results and the interaction of these salts with the model peptide compound acetyltetraglycine ethyl ester, described by Robinson and Jencks.

Acetates↗

PubMed1996

Fluid, ionic and hormonal changes induced by high salt intake in salt-sensitive and salt-resistant hypertensive patients.

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin-aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 +/- 35 to 226 +/- 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 +/- 76 to 364 +/- 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 +/- 0.11 to 1.56 +/- 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 +/- 0.08 to 1.12 +/- 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

Aldosterone↗

PubMed2001

The calciuric response to dietary salt of Dahl salt-sensitive and salt-resistant female rats.

BACKGROUND: We have shown previously that the calciuric response to salt does not differ in Dahl salt-sensitive (S) and salt-resistant (R) male rats. Clinical studies with women, however, suggest an effect of salt sensitivity on the calciuric response to salt. The objective of this study was to determine whether there is an effect of salt sensitivity on the calciuric response to salt of female S and R rats. METHOD: Dahl S and R female rats were fed high- (8%) or low- (0.3%) salt diets for 3 weeks. The rats were placed in metabolic cages for 24-hour urine collection at baseline and weekly (for sodium and calcium determination). RESULTS: Blood pressure of female S rats was 177+/-3.0 mm Hg at week 3 of high salt intake compared with 96+/-1 mm Hg for female R rats. Female S rats excreted significantly more calcium than female R rats at baseline (P < 0.001), when fed a nonpurified diet, and during high salt intake (P = 0.004). Salt sensitivity significantly increased calcium excretion, water intake, and urine output when rats were fed a high-salt diet. Calcium excretion, water intake, and urine output of female S rats were time-dependent during high salt intake. Plasma 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations were markedly lower in female S rats fed a high-salt diet, but not in female R rats. Plasma parathyroid hormone and 1,25-dihydroxyvitamin D concentrations did not significantly differ between female S and R rats, but plasma concentrations of these two hormones at week 3 were significantly higher in S rats fed a high-salt diet compared with S rats fed a low-salt diet. CONCLUSIONS: Our data indicate that the calciuric response to salt is greater in female S compared with female R rats, thus supporting findings on the effect of salt sensitivity reported in several clinical studies with women. The greater calciuric response to salt of female S rats compared with female R rats, which was not seen in a previous study when male S rats were compared to male R rats, suggest a gender difference in the calciuric response to salt.

Animals↗

PubMed1992

High salt diet down-regulates proximal tubule Na+, K(+)-ATPase activity in Dahl salt-resistant but not in Dahl salt-sensitive rats: evidence of defective dopamine regulation.

We examined the regulation of Na+,K(+)-ATPase activity in proximal tubule segments during a high salt diet in prehypertensive Dahl salt-sensitive and salt-resistant rats. Rats were placed on normal salt or high salt diets (0.9% saline as drinking water). During the normal salt diet, Na+,K(+)-ATPase activity was not different between Dahl salt-sensitive and salt-resistant rats. After 2 days and 10 days on a high salt diet, Na+,K(+)-ATPase activity in Dahl salt-resistant rats significantly decreased when compared to Dahl salt-resistant rats on a normal salt diet (P less than 0.01). The decreased Na+,K(+)-ATPase activity in Dahl salt-resistant rats during a high salt diet was reversed by treatment with an inhibitor of aromatic L-amino acid decarboxylase (dopamine synthesizing enzyme), benserazide. In contrast, Na+,K(+)-ATPase activity did not decrease during the high salt diet and benserazide had no effect on Na+,K(+)-ATPase activity in Dahl salt-sensitive rats. These results indicate that Dahl salt-sensitive rats do not have the capacity to down-regulate the proximal tubule Na+,K(+)-ATPase activity during a high salt diet. Indirect evidence suggests that the regulation of Na+,K(+)-ATPase activity by locally produced dopamine is absent in Dahl salt-sensitive rats.

Animals↗

PubMedDate not supplied

Bile salt structure and phase equilibria in aqueous bile salt and bile salt-lecithin systems.

The hydrophilic-hydrophobic balance of bile salt monomers can be readily quantified by their elution sequence during reverse-phase high-performance liquid chromatography. Such studies have demonstrated that subtle variations in bile salt structure have profound effects on the hydrophilic-hydrophobic balance of this important family of detergent-like molecules. The common trihydroxy bile salt, cholate, is more hydrophilic than dihydroxy bile salts with alpha-oriented OH groups. In contrast, dihydroxy bile salts with one equatorial OH function are more hydrophilic than cholate. Hydrophilic bile salts have, in general, higher critical micellar concentrations than do hydrophobic bile salts and their primary micelles polymerize less readily to form secondary micelles either with increasing bile salt concentrations or with increases in ionic strength. Hydrophilic bile salts also disperse lecithin into mixed micelles at a slower rate than do hydrophobic bile salts. The structure of mixed bile salt-lecithin micelles is more complex than previously believed and varies with bile salt-to-lecithin ratio. These micelles are disc-like in which bile salts saturate the lecithin bilayer "core" presumably as reverse micelles, as well as coating the perimeter as a bilayered "ribbon". The ratio of bile salt to lecithin in the bilayer and the intermicellar monomeric bile salt concentration (critical micellar concentration) determines the macroscopic phase limit. With the common bile salt species, the lecithin-to-bile salt phase limit does not correlate closely with the hydrophilic-hydrophobic balance of the bile salt monomers.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed2001

The calciuric response to dietary salt of Dahl salt-sensitive and salt-resistant male rats.

BACKGROUND: There are conflicting reports regarding the effect of salt sensitivity on the calciuric response to salt, perhaps because of gender differences and different modes of salt administration. We tested the hypothesis that the calciuric response to dietary salt would not differ for male Dahl salt-sensitive (S) and salt-resistant (R) rats. METHOD: S and R rats were fed high- (80 g/kg) or low- (3 g/kg) salt diets for 3 weeks and urine (24 hour) was collected weekly. RESULTS: Urinary calcium excretion was up to 20-fold greater for S and R rats fed a high-salt diet (P < 0.001) than for S and R rats fed a low-salt diet and did not differ significantly between S and R rats. S rats, however, excreted calcium in significantly higher urine volumes (P< 0.001) during high salt intake and developed hypertension. Plasma parathyroid hormone concentrations of S and R rats did not differ during low salt intake and increased significantly to the same concentration after 3 weeks of high salt intake. CONCLUSIONS: We have previously reported that plasma 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations of male S rats, but not male R rats, were drastically reduced by 3 weeks of high salt intake. These data suggest that salt-induced hypertension and salt-induced alterations in the vitamin D endocrine system of male S rats do not affect the calciuric response to dietary salt.

Animals↗

PubMed1987

Morphometric evaluation of the renal arterial system of Dahl salt-sensitive and salt-resistant rats on a high salt diet. I. Interlobar and arcuate arteries.

Structural changes in intrarenal arteries of inbred Dahl salt-sensitive and salt-resistant rats with acute hypertension were studied morphometrically. After a week on a normal salt diet (1% NaCl), animals were placed on a high salt diet (8% NaCl) for 4 weeks. Systolic blood pressure (BP) and body weights (BW) were recorded, and six salt-sensitive and six salt-resistant animals were sacrificed weekly for a total of five sampling periods. Corrected cross-sectional (C/S) areas of adventitia, media (MAC), intima, wall (WAC), and lumen (LAC) were measured by planimetry. Although significant increases (p less than 0.01) in both BW and systolic BP were observed over time in both strains, salt-sensitive rats became hypertensive (systolic BP greater than 150 mm Hg) by week 2 on a high salt diet, while salt-resistant rats remained normotensive. In interlobar arteries, significant increases over time were observed for the WAC, MAC, and LAC in salt-resistant rats and in the WAC, adventitia, MAC, and LAC for salt-sensitive rats. Significant increases over time were observed for the WAC, adventitia, MAC, and LAC in arcuate arteries from salt-sensitive rats only. Increased C/S areas observed over time in both strains were observed by week 3 on the high salt diet, after the elevated systolic BP. Analysis of covariance indicated that increased C/S areas observed over time in salt-sensitive rats paralleled elevated systolic BP but did not follow an increase in BW. On the other hand, in salt-resistant rats, increased C/S areas observed over time correlated with BW but not systolic BP. The documented rapid development of vascular changes in salt-sensitive rats in conjunction with the development of acute hypertension demonstrates the potential usefulness of this model for investigating the pathogenesis of hypertensive renal vascular alterations.

Animals↗

PubMed1992

Preferred salt levels and salt taste acuity in human subjects after ingestion of untasted salt.

We have examined whether salt loading alters the salt preference or salt taste acuity of nine human subjects on continuous low salt diet. Subjects were randomly assigned to either untasted salt tablets (120 mmol/day) or placebo over a 2-week period at the end of which salt preference and salt recognition thresholds were measured. Subjects then received the alternate substance for another 2 weeks and the measurements were repeated. While urinary Na+ and Cl- were significantly increased while on salt tablets, urinary volume, K+, urea and creatinine concentrations, blood pressure, body weight, salivary and plasma electrolyte concentrations were unchanged. Plasma renin and aldosterone levels were reduced while on salt tablets but not significantly. Salt tablets caused a significant increase in sodium recognition threshold but a significant decrease in salt addition to unsalted tomato juice and in ideal salt level assessed by presalted (150 mmol/l) tomato juice. Thus, an increase in untasted dietary salt may reduce salt preference in human subjects, a finding opposite to that with an increased, tasted salt intake over a similar period.

Adult↗

PubMed1992

The Salt Step Test: its usage in the diagnosis of salt-sensitive hypertension and in the detection of the salt hypertension threshold.

The Salt Step Test was devised to characterize the response of the hypertensive patient to dietary salt. The test has three phases: unrestricted salt, to document hypertension and customary salt intake; restricted salt (2 g/day), to identify the salt-sensitive patient; and stepwise increased salt (each step = 1 g/day), to find the level that precipitates hypertension. The Salt Step Test identified that out of 30 well-established adult hypertensives, 13 were salt-sensitive. It also revealed that in each salt-sensitive patient, a distinct level of salt (range 3-16 g/day) precipitated hypertension, i.e., a Salt Hypertension Threshold. Definition of the Salt Hypertension Threshold should be useful in providing specific, individualized guidelines for dietary salt restriction.

Adult↗

PubMed1989

Various sodium salts, potassium salts, a calcium salt and an ammonium salt induced ornithine decarboxylase and stimulated DNA synthesis in rat stomach mucosa.

Studies were made on the possible tumor-promoting activities of various salts of food additives in the glandular stomach mucosa of F344 male rats after their administration by gastric intubation. Up to 100-fold increases in ornithine decarboxylase (ODC) activity in the pyloric mucosa of the stomach with maxima after 8 h were observed after administration of sodium acetate at doses of 3.68-13.6 mmol/kg body weight, sodium L-ascorbate at doses of 8.55-17.1 mmol/kg body weight, Na2CO3 at doses of 4.73-14.2 mmol/kg body weight, sodium L-glutamate at doses of 12.8-17.1 mmol/kg body weight, sodium sorbate at doses of 8.92-17.1 mmol/kg body weight and (NH4)2SO4 at doses of 7.56-20.1 mmol/kg body weight. Increases of up to 100-fold in ODC activity with maxima after 16 h were also observed after intubation of KCl at doses of 10.1-22.0 mmol/kg body weight, K2SO3 at doses of 2.84-8.45 mmol/kg body weight, K2S2O5 at doses of 2.25-6.75 mmol/kg body weight and CaCl2 at doses of 2.0-4.08 mmol/kg body weight. Sodium acetate at a dose of 11.0 mmol/kg body weight, KCl at a dose of 20.1 mmol/kg body weight, K2S2O5 at a dose of 5.40 mmol/kg body weight and CaCl2 at a dose of 3.4 mmol/kg body weight induced up to 10-fold increase in DNA synthesis in the pyloric mucosa of the stomach with maxima after 16-24 h. These results suggest that these salts of food additives may, like NaCl, have tumor-promoting activities in the pyloric mucosa of rat stomach.

Animals↗

PubMed1998

Determination of discretionary salt intake in rural Guatemala and Benin to determine the iodine fortification of salt required to control iodine deficiency disorders: studies using lithium-labeled salt.

The use of discretionary salt, which is salt added during cooking and at the table, as a suitable vehicle for iodine intake was assessed by measuring salt consumption using the lithium-marker technique in rural areas of Guatemala and Benin. In both countries, we studied boys aged 6-12 y and their mothers. Subjects used lithium-labeled salt after all unlabeled salt was removed from their households. In Guatemala, 24-h urine samples for 9 mother-son pairs were collected at baseline and on days 7, 8, and 9 during the use of lithium-labeled salt. Total maternal salt intake averaged 5.2 +/- 1.7 g/d (mean +/- SD), of which 77 +/- 24% came from discretionary sources, whereas Guatemalan boys consumed 1.8 +/- 0.6 g salt/d, of which 72 +/- 12% came from discretionary sources. In Benin, urine collection from 13 mother-son pairs took place at baseline and on days 5 and 7. Beninese mothers had a total salt intake of 9.0 +/- 2.9 g/d and their sons had an intake of 5.7 +/- 2.8 g/d; discretionary salt contributed 52 +/- 14% and 50 +/- 13%, respectively, of total salt consumed. Therefore, fortification of household salt appears to be an appropriate method of controlling iodine deficiency in both countries, although fortification of other salt sources could be considered in Benin.

Adult↗

PubMed1987

Effects of salt loading on the fractional volume of atria-specific granules in Dahl salt-sensitive and salt-resistant rats.

The cardiac atria are known to play a role in blood volume homeostasis, secreting a peptide that induces a potent natriuresis and diuresis. This peptide is atrial natriuretic factor (ANF), and its primary site of storage is within atria-specific granules found in atrial cardiocytes. Since salt loading results in an increase in circulating levels of ANF, our aim was to determine if the atria-specific granule population in the cardiocytes of Dahl rats would decrease accordingly. To this end, the fractional volume of the atria-specific granules was determined by ultrastructural morphometric analysis in the Dahl salt model of hypertension. This analysis was performed on the right atria of Dahl Salt-resistant (DR) and salt-sensitive (DS) rats fed either a low-salt (0.4%) or high-salt (8%) diet for 12 weeks prior to sacrifice. DR and DS rats fed a low-salt diet had significantly reduced plasma sodium levels and osmolalities, and a significantly lower mean arterial blood pressure than did rats fed a high-salt diet. The fractional volume of atria-specific granules was significantly lower in salt-loaded DR (P less than 0.01) and DS (P less than 0.025) rats than in their respective low-salt controls. This significant decrease in atrial granules corresponds to the reported decrease in the storage of atrial ANF in salt-loaded rats, and provides a morphological verification of the biochemical studies. Moreover, these results, in combination with a growing body of physiological data, lend support to the hypothesized role of ANF in the regulation of water-electrolyte balance, which may play an important role in cardiovascular pathophysiological states related to hypertension.

Animals↗

PubMed1990

Salt intake and renal hemodynamics in immature and mature Dahl salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats.

To determine if abnormalities in the maturation of renal function in Dahl salt-sensitive rats are associated with the development of hypertension, studies were performed in anesthetized 3 week old salt-sensitive (DS/JR) and salt-resistant (DR/JR) rats whose mothers were maintained on 0.15% (low-salt) during gestation and either 0.15% or 2.0% (high-salt) NaC1 diets after parturition. Mature DS/JR and DR/JR rats were maintained on either 0.15% or 2.0% NaC1 diets after weaning and studied at 8 to 9 weeks of age. High-salt diet raised blood pressure (BP) and reduced glomerular filtration rate (GFR) and renal blood flow (RBF) in mature DS/JR rats, but had no effect on BP, GFR and RBF in mature DR/JR rats. In immature DS/JR and DR/JR animals, high-salt intake resulted in poor growth with reductions in GFR and RBF in the DS/JR group. The response to acute volume expansion, (5% body weight physiologic saline infusion) differed among the groups. Mature rats all vasodilated while immature high-salt DS/JR did not, and immature low-salt DS/JR vasoconstricted. These studies demonstrated that both mature and immature DS/JR rats evidence abnormal responses to acute and chronic salt loading. Early exposure to high-salt intake affects the maturation of renal function in the DS/JR group. An enhanced vascular sensitivity to sodium is present at critical periods of postnatal development in DS/JR rats.

Animals↗

PubMed1993

Effects of a high-salt diet on hepatic atrial natriuretic peptide receptor expression in Dahl salt-resistant and salt-sensitive rats.

OBJECTIVE: To investigate the effects of a salt diet and of salt-induced hypertension on hepatic atrial natriuretic peptide (ANP) receptors in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats. METHODS: DS and DR rats were maintained for 5 weeks on either normal- (0.8% w:w NaCl) or high- (8% w:w NaCl) salt diets. Blood pressures were recorded by a tail-cuff analyser and plasma ANP concentrations were determined by radioimmunoassay. ANP binding and guanylate cyclase activities in purified liver plasma membrane fractions were determined by conventional radioreceptor and enzymatic techniques. RESULTS: DS rats exhibited higher blood pressure than DR rats on the equivalent diet and in both groups the high-salt diet significantly increased systolic blood pressures. The high-salt diet significantly reduced plasma ANP concentrations in DR rats but not DS rats. Membrane fractions from DS rats exhibited increased ANP receptor densities compared to membranes isolated from DR rats on the equivalent diet. The high-salt diet induced a significant increase in receptor density in the DS but not the DR group. The fractional displacement of [125I]-ANP binding by the truncated, ring-deleted analogue des[QSGLG]-4,23-ANP-NH2 was reduced in membrane fractions isolated from DS rats maintained on the high-salt diet. There was no change in ANP receptor affinity. Increases in receptor density in DS rats were accompanied by increases in both basal and ANP-stimulated guanylate cyclase activities. CONCLUSIONS: These results indicate that plasma membrane isolated from the liver of DS rats exhibit increased expression of the guanylate cyclase-linked ANP-B (guanylate cyclase-A and/or guanylate cyclase-B) receptors over similar preparations isolated from DR rats. ANP B receptor density is further increased when DS rats are maintained on a high-salt diet.

Animals↗

PubMed1989

Differential effect of dietary salt on renal growth in Dahl salt-sensitive and salt-resistant rats.

A high salt diet has been shown to increase renal mass of intact rats, although the mechanism by which this occurs has not been investigated. We used Dahl rats that are sensitive (DS) or resistant (DR) to the hypertensinogenic effect of salt to examine changes in renal size and composition caused by a high salt diet. Renal index, deoxyribonucleic acid (DNA), protein, water content, protein/DNA ratio, and cell number and size were measured in age-matched DR and DS on a high salt diet for 7, 14, or 28 days. The results were compared with those obtained from respective rats on a low salt diet. High salt diet elevated renal index and protein in DR and DS rats at each time point. After 7 days of a high salt diet, DNA increased in DS only. Protein/DNA ratio was progressively decreased by a high salt diet in DS and remained unchanged in DR rats. Cell number was increased 35% in DS versus only 13% in DR rats at 4 weeks. Cell size decreased 24% in DS and only 11% in DR rats. These results indicate that renal growth due to hyperplasia accompanies ingestion of a high salt diet in both DR and DS rats, but the rate of growth and the mechanism through which it occurs differ between strains. This difference may be important in delineating salt sensitivity and future development of hypertension.

Animals↗

PubMed1998

Insulinemia and pancreatic alpha2-adrenoceptors in salt-sensitive (SBH) and salt-resistant (SBN) Sabra rats: effect of high salt diet.

Studies in humans have suggested that hyperinsulinemia might play an important role in salt sensitivity and in the later development of high blood pressure. This possibility has been tested in this study on Sabra rats, an animal model of salt-induced hypertension. Salt-sensitive (SBH) and salt-resistant (SBN) Sabra rats have been submitted to either a normal (0.2% NaCl) or a high salt (8% NaCl) diet for 6 weeks. Comparisons of blood pressure, basal glucose and insulin levels, and insulin response to glucose overload (1 g/kg) have been made. As pancreatic alpha2-adrenergic receptors are implicated in the control of insulin release, their densities have been determined on plasma membranes by saturation studies with [3H]-RX-821002 as the specific radioligand. Under normal diet, blood pressures were respectively 133 +/- 9 and 108 +/- 10 mm Hg (n = 6) in SBH and SBN. Basal glucose and insulin levels and insulin response to glucose overload were found to be significantly higher in SBH than in SBN. In contrast, alpha2-adrenergic receptor densities were lower (P < .001) in SBH when compared to SBN. High salt diet increased (P < .01) blood pressure, decreased basal glucose (P < .01) and insulin (P < .001) levels only in SBH. However, when compared to SBN the insulin response to glucose overload was maintained higher in SBH. Alpha2-adrenergic receptor densities and difference between SBH and SBN did not differ from those found in normal diet. In conclusion, the salt-induced high blood pressure of salt-sensitive Sabra rats is not associated with hyperinsulinemia and insulin resistance. Indeed, an improvement in the insulin sensitivity appears to be induced by either a high salt diet or high blood pressure.

Animals↗

PubMed1983

Recovery of salt appetite after lateral hypothalamic lesions: effects of preoperative salt drive and salt intake experiences.

This study presents further observations on the effects of preoperative salt experiences on salt appetite following lesions of the lateral hypothalamus. The results confirmed earlier findings that preoperative salt experiences can protect the rat against the usual deficit in regulatory salt intake that follows such lesions. However, the results suggested that there may be no specific feature of the preoperative salt experience that is critical for the protective effect since both salt drive experience without concomitant salt intake experience and salt intake experience without concomitant salt drive experience were effective.

Animals↗

PubMed2000

Salt appetite in salt-replete rats: involvement of mesolimbic structures in deoxycorticosterone-induced salt craving behavior.

Chronic administration of the mineralocorticoid deoxycorticosterone acetate (DOCA) induces a steady and robust increase in salt appetite and plasma Na(+) over the course of treatment. Interestingly, salt appetite behavior persists in rats even with elevated plasma Na(+) levels. Since there is evidence that the pathways normally associated with salt and water homeostasis are relatively unaffected in the DOCA-treated rat, we hypothesized that other regulatory systems may be hyperactive giving rise to this dysfunctional condition. The mesolimbic dopaminergic system has long been associated with orienting and reward-seeking behaviors such as those observed in reproduction, drug abuse, and appetite. Furthermore, we have previously shown that chronic DOCA administration results in an increase in mRNA levels of the endogenous opiate enkephalin in male rats given 24-hour access to tap water and 2% NaCl (two-bottle choice). Thus, in the present study, we tested the hypothesis that the mesolimbic dopaminergic system is dysfunctionally sensitized to the presence of a salt stimulus in DOCA-treated animals. Four groups of rats were injected with DOCA (5 mg/rat/day, 11 days) and one with vehicle (all were given access to water but access to salt was regulated). Two DOCA groups were given 2 h of 2% NaCl access/day and on the last day, one group was not given access (2hX). One of the two remaining DOCA groups was given 24-hour access to salt (24h) and the other no access at all (24hX). Consistent with our hypothesis, in the shell of the nucleus accumbens (AcbSh) we found relatively higher enkephalin- and tachykinin-mRNA abundance in the 2h vs. 2hX and dynorphin-mRNA in the 24h vs. 24hX groups. In addition, there were decreases in dopamine transporter binding in the AcbSh and decreases in tyrosine hydroxylase immunoreactivity throughout the striatum in the 24h vs. 24hX group. Furthermore, rats denied access to salt (2hX and 24hX) had higher cholecystokinin-mRNA levels in the ventral tegmental area compared to the 2h and 24h groups, respectively. These results suggest that basal ganglia structures associated with reward and goal-seeking behavior may be activated to elicit salt craving behavior in the DOCA-induced salt-appetitive rat.

Animals↗