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PubMed1989

Salt intake and plasma renin activity in the freshwater turtle.

In mammals, a well-documented inverse relationship exists between oral salt intake and plasma renin activity (PRA). We carried out this study to determine if a similar relationship exists in the freshwater turtle Pseudemys scripta. Three groups of turtles (N = 8 for each group) were fed different amounts of salt dissolved in distilled water (2 cc/kg). The high salt group received 580 mg (10 mEq) NaCl/kg twice per week, the medium salt group received 290 mg (5 mEq) NaCl/kg twice per week, and the low salt (control) group received 2 cc/kg distilled water twice per week with no salt. The animals were weighed weekly and blood was collected by cardiac puncture after 3 and 6 weeks of salt loading and again 3 weeks after termination of the salt loading. PRA and plasma electrolytes (PNa, PK, PCl) were determined. The low salt (control) group showed no changes in any of the measured variables throughout the 9-week study. At 3 weeks the following mean values were obtained for the control group: PNa, 119.5 +/- 7.2 mEq/liter; PK, 5.0 +/- 1.0 mEq/liter; PCl, 74.1 +/- 2.6 mEq/liter; PRA, 1.0 +/- 0.2 ng/ml/hr. In the medium salt group, no significant changes were seen until 3 weeks after termination of the salt loading when PNa and PRA were elevated to 137.9 +/- 3.6 mEq/liter and 1.9 +/- 0.2 ng/ml/hr, respectively (P less than 0.05 compared to control). In the high salt group, PNa (136.5 +/- 6.5 mEq/liter) was elevated after 3 weeks of salt loading. At 6 weeks, PNa (136.8 +/- 4.9 mEq/liter) remained elevated in the high salt group and PCl (86.3 +/- 1.3 mEq/liter) and PRA (1.7 +/- 0.2 ng/ml/hr) also increased significantly (P less than 0.05 compared to control in each case). Three weeks after termination of salt loading, PNa (136.8 +/- 3.3 mEq/liter). PCl (88.0 +/- 1.6 mEq/liter), and PRA (1.9 +/- 0.2 ng/ml/hr) remained elevated (P less than 0.05 in each case) in the high salt group while PK dropped to 3.5 +/- 1.6 mEq/liter (P less than 0.05). The results show that after 6 weeks of salt loading sufficient to raise PNa in the turtle, PRA was significantly elevated.

Animals↗
PubMed2006

Increased levels of atherosclerosis markers in salt-sensitive hypertension.

BACKGROUND: Salt sensitivity in essential hypertension is associated with both endothelial dysfunction and increased cardiovascular risk. We evaluated several serum markers of atherosclerosis and endothelial function in a group of essential hypertensive patients classified on the basis of their salt sensitivity. METHODS: Forty-three patients were classified as having salt-sensitive (20 subjects) or salt-resistant (23 subjects) hypertension on the basis of their 24-h blood pressure (BP) response from low salt (50 mmol/d) to high salt (250 mmol/d) intake. Endothelium-dependent and independent responses were measured in the forearm previously to salt manipulation. High-sensitivity C-reactive protein (CRP), soluble intercellular adhesion molecule type 1 (sICAM-1), soluble vascular cell adhesion molecule type 1 (sVCAM-1), e-selectin, p-selectin, interleukin-6 (IL-6), monocyte chemotactic protein type 1 (MCP-1), matrix metalloproteinases types 1, 2, and 9 (MMP-1, MMP-2, and MMP-9), and the tissue inhibitor of metalloproteinases type 1 (TIMP-1) were measured in serum on the last day of both low salt and high salt intakes. RESULTS: Compared to salt-resistant patients, salt-sensitive hypertensives showed age-adjusted increased levels of p-selectin (P = .006), e-selectin (P = .042), and MCP-1 (P = .036), although differences in e-selectin were not maintained after adjustment for BP values. Moreover, salt-sensitive subjects exhibited decreased serum levels of MMP-9 (P = .007) and increased levels of TIMP-1 (P = .045). No differences in serum CRP, sICAM-1, sVCAM-1, or IL-6 were observed between salt-sensitive and salt-resistant patients. Finally, maximal acetylcholine-induced vasodilation (319% +/- 153% v 414% +/- 178% increase in forearm blood flow; P = .022 age-adjusted) was significantly impaired in salt-sensitive hypertensives. CONCLUSIONS: Serum markers of inflammation, especially selectins and chemokines, as well as markers of vascular remodeling, and endothelium-dependent vasodilation are altered in salt-sensitive hypertension. These alterations could help to explain the greater target organ damage and cardiovascular risk observed in salt-sensitive subjects.

Adult↗
PubMed2001

Preparation and characterisation of a range of diclofenac salts.

Physicochemical properties of diclofenac salts prepared using eight different counterions and including five novel salts, obtained with the bases 2-amino-2-methyl-1,3-propanediol, 2-amino-2-methylpropanol, tert-butylamine, benzylamine and deanol, were compared. Four of the bases used to prepare these salts were related in their chemical structure, differing only in the number of hydroxy groups. Characterisation techniques included X-ray diffraction, differential scanning calorimetry, thermogravimetric analysis, thermomicroscopy, Karl Fischer titration, FT-IR spectroscopy and elemental analysis. In the case of salts prepared from 2-amino-2-methylpropanol and benzylamine, two polymorphic forms of each salt were identified. For the 2-amino-2-methyl-1,3-propanediol salt, a pseudopolymorphic form was identified. The aqueous solubilities of the salts studied ranged from 3.95 mM (tris(hydroxymethyl)aminomethane salt) to 446 mM (deanol salt), corresponding to a 113-fold difference in solubility. The solubility of diclofenac deanol was higher than the solubilities for diclofenac salts reported earlier. Correlation was found between the inverse of the salt melting point and the logarithm of salt solubility. A log-log relationship was observed between salt solubility and hydrogen ion concentration in the salt solution. Relationships between the properties of the salt-forming agents and those of the resulting diclofenac salts were explored. Reasonable correlation was found between the free base melting point and the salt melting point.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Effect of salt intake on jejunal dopamine, Na+,K+-ATPase activity and electrolyte transport.

The present study addresses the question of the relevance of salt intake on jejunal dopamine, Na+,K+-ATPase activity and electrolyte transport. Low salt, but not high salt, intake for 2 weeks increased dopamine levels in the jejunal mucosa accompanied by a marked decrease in L-3,4-dihydroxyphenylalanine tissue levels. By contrast, in rats fasted for 72 h the effect of refeeding for 24 h with a low salt diet failed to change dopamine tissue levels, although it significantly increased those of L-3,4-dihydroxyphenylalanine. By contrast, high salt intake markedly increased the tissue levels of both dopamine and L-3,4-dihydroxyphenylalanine, without changes in dopamine/L-3,4-dihydroxyphenylalanine tissue ratios. Tissue levels of both L-3,4-dihydroxyphenylalanine and dopamine in control conditions (normal salt intake for 2 weeks) were markedly higher (P < 0.05) than in rats submitted to 72 h fasting plus 24 h refeeding. The effect of fasting for 72 h followed by 24 h refeeding was a marked decrease in jejunal Na+,K+-ATPase activity, particularly evident for rats fed a normal salt and high salt diets during the refeeding period. Basal short circuit current was similar in rats fed a normal salt diet for 2 weeks and 24 h, and the type of diet failed to alter basal short circuit current after refeeding with normal, low and high salt diets. On the other hand, the effect of prolonged low salt intake was a marked decrease in jejunal Na+, K+-ATPase activity and basal short circuit current, whereas high salt intake failed to alter enzyme activity and basal short circuit current. In rats fed for 2 weeks a high salt diet ouabain was found to be more potent in reducing jejunal short circuit current than in rats fed normal and low salt diets. The effect of furosemide was more marked in rats fed for 2 weeks high and low salt diets than in animals receiving a normal salt intake. Dopamine (up to 1 micromol L-1) was found not to alter Na+,K+-ATPase and basal short circuit current in jejunal epithelial sheets, in rats fed with normal, low and high salt diets for 2 weeks and 24 h.

Animal Feed↗
PubMed1999

High salt intake potentiates the renal vascular and glomerular damage caused by low doses of angiotensin II in uni-nephrectomized rats.

OBJECTIVE: We recently reported that the renin-angiotensin system plays an important role in the progression of vascular and kidney injuries, even in Dahl salt-sensitive rats with volume-dependent hypertension. In this study, we investigated whether a high-salt diet increases susceptibility to kidney injury induced by angiotensin II in normotensive, uni-nephrectomized Sprague-Dawley rats, which mimics the condition of salt-volume repletion and blunted renin-angiotensin system. METHODS: The rats were fed either a low-salt (0.3% NaCl) or a high-salt (4% NaCl) diet and divided into five groups: two control groups with a low-salt or a high-salt diet without angiotensin II infusion (saline infusion), and three angiotensin II groups (angiotensin II infusion, 10 or 50 ng/kg per min with high-salt diet, 50 ng/kg per min with low-salt diet, subcutaneously). The rats were kept on these regimes for 8 weeks. The blood pressure was measured every week. Functional and morphological alterations in the kidney were assessed at the end of the experiment RESULTS: There were no differences in the arterial blood pressures of the five experimental groups. However, angiotensin II infusion increased the weights of the heart and aortic walls in a dose-dependent manner in the high-salt groups. There was also a dose-dependent increase in proteinuria, N-acetyl-beta-D-glucosaminidase activity (NAG) excretion, and additional glomerular and arterial injuries in the kidney, associated with angiotensin II infusion in the high-salt groups. In the rats given a higher dose of angiotensin II, the high-salt diet significantly increased the weights of the heart and aortic walls and exacerbated the renal function and morphological injuries, compared to the low-salt group. High-salt diet alone increased the kidney and heart weights. However, it did not significantly influence the results of the morphological and functional study. On the other hand, angiotensin II infusion on a low-salt diet showed a trend towards glomerular damage; however, the effects were small and not significant. Similarly, there were few effects of angiotensin II infusion on morphology and functional study on a low-salt diet CONCLUSION: These data clearly show that a high-salt intake increases susceptibility of the kidney to injuries induced by low doses of angiotensin II in normotensive, uni-nephrectomized rats.

Angiotensin II↗
PubMed2004

Salt cress. A halophyte and cryophyte Arabidopsis relative model system and its applicability to molecular genetic analyses of growth and development of extremophiles.

Salt cress (Thellungiella halophila) is a small winter annual crucifer with a short life cycle. It has a small genome (about 2 x Arabidopsis) with high sequence identity (average 92%) with Arabidopsis, and can be genetically transformed by the simple floral dip procedure. It is capable of copious seed production. Salt cress is an extremophile native to harsh environments and can reproduce after exposure to extreme salinity (500 mm NaCl) or cold to -15 degrees C. It is a typical halophyte that accumulates NaCl at controlled rates and also dramatic levels of Pro (>150 mm) during exposure to high salinity. Stomata of salt cress are distributed on the leaf surface at higher density, but are less open than the stomata of Arabidopsis and respond to salt stress by closing more tightly. Leaves of salt cress are more succulent-like, have a second layer of palisade mesophyll cells, and are frequently shed during extreme salt stress. Roots of salt cress develop both an extra endodermis and cortex cell layer compared to Arabidopsis. Salt cress, although salt and cold tolerant, is not exceptionally tolerant of soil desiccation. We have isolated several ethyl methanesulfonate mutants of salt cress that have reduced salinity tolerance, which provide evidence that salt tolerance in this halophyte can be significantly affected by individual genetic loci. Analysis of salt cress expressed sequence tags provides evidence for the presence of paralogs, missing in the Arabidopsis genome, and for genes with abiotic stress-relevant functions. Hybridizations of salt cress RNA targets to an Arabidopsis whole-genome oligonucleotide array indicate that commonly stress-associated transcripts are expressed at a noticeably higher level in unstressed salt cress plants and are induced rapidly under stress. Efficient transformation of salt cress allows for simple gene exchange between Arabidopsis and salt cress. In addition, the generation of T-DNA-tagged mutant collections of salt cress, already in progress, will open the door to a new era of forward and reverse genetic studies of extremophile plant biology.

Abscisic Acid↗
PubMed2004

Urinary excretion rate of Tamm-Horsfall protein is related to salt intake in humans.

BACKGROUND/AIMS: Increased salt intake and enhanced salt sensitivity are implicated in the pathogenesis of hypertension. The aim of the present study was to investigate whether the urinary excretion rate of Tamm-Horsfall protein (THP) is dependent on salt intake in healthy, genetically hypertension-prone individuals. METHODS: Thirty unrelated subjects (13 men and 17 women, mean age 48.1 +/- 6.7 years) with at least one first-degree relative with primary hypertension were studied. After a baseline investigation, the study subjects were put on a low-salt diet (10 mmol of sodium and 70 mmol of potassium per day) for 1 week. During the second week, sodium chloride capsules (230 mmol/day) were added to the diet to achieve a high-salt intake of 240 mmol/day. Urine samples (24-hour and overnight collections) were collected before the baseline investigation and at the end of the high- and low-salt diet weeks. The salt sensitivity was calculated as the difference between the blood pressure during high salt intake and the blood pressure during low salt intake. RESULTS: A low salt intake induced a decrease in the urinary excretion rate of THP during the night (11.7 microg/min) compared with baseline (19.5 microg/min; p < 0.05) and high salt intake (23.1 microg/min; p < 0.01). Furthermore, a greater response in blood pressure to a high salt intake, i.e. high salt sensitivity, was associated with increased excretion of THP in urine during the change to high salt intake (r = 0.38, p < 0.05). CONCLUSION: We were able to confirm that urinary excretion of THP is dependent on sodium intake. Patients with a high salt sensitivity, i.e. an exaggerated blood pressure response to high salt intake, responded to the high salt intake with an even greater increase in the urinary excretion rate of THP. The mechanism underlying this response is still unknown, but it might indicate that distal nephron function in healthy, genetically hypertension-prone individuals is altered.

Blood Pressure↗
PubMed1990

Effect of dietary salt on the skeletal muscle microvasculature in Dahl rats.

The purpose of this study was to identify microvascular alterations that could contribute to increased peripheral vascular resistance in the Dahl salt-sensitive rat with salt-induced hypertension. Intravital microscopy was used to study the spinotrapezius muscle arteriolar network in anesthetized salt-sensitive rats fed either a high salt (7% sodium chloride) or low-normal salt (0.45% sodium chloride) diet for 4 weeks. Age-matched Dahl salt-resistant rats on high and low-normal salt diets served as controls. The high salt diet had no effect on arterial pressure in salt-resistant rats but increased arterial pressure in salt-sensitive rats. Mean resting diameter of arcade arterioles in salt-sensitive rats on high salt diet was reduced by 25% compared with salt-sensitive rats on low salt or salt-resistant rats on either diet. After abolition of vascular tone with 10(-3) M adenosine, arcade diameters were comparable in all groups. No difference among groups was found in either resting or passive diameter of the more distal transverse arterioles. Measurement of vessel lengths and numbers in cleared muscle specimens revealed no differences among groups in the anatomic density of either arcade or transverse arterioles. These data suggest that a reduction in the resting diameter of arcade, but not transverse, arterioles may increase spinotrapezius muscle vascular resistance in hypertensive salt-sensitive rats. The similarity in vascular densities among groups indicates that structural rarefaction of arterioles does not contribute to any increase in spinotrapezius muscle resistance at this stage of salt-induced hypertension.

Adenosine↗
PubMed1990

Salt sensitivity in humans is associated with abnormal acid-base regulation.

Metabolic acidosis has recently been observed in rat models of salt-sensitive genetic hypertension. To test the hypothesis that salt sensitivity in humans may be associated with abnormal acid-base homeostasis, we performed arterial blood gas analyses in young (20-31 years old) normotensive subjects (n = 40) who were placed on a low salt diet (20 mmol NaCl/day) for 2 weeks with either 200 mmol sodium chloride or placebo added to the low salt diet for 1 week each in a randomized, single-blind crossover order. Furthermore, a subset of the subjects (seven salt-sensitive and eight salt-resistant) received 200 mmol sodium/day as the citrate salt as a supplement to the low salt diet for a third week. During each regimen, blood pressure as well as arterial pH and bicarbonate levels were measured. Salt sensitivity was defined as a significant drop in mean arterial pressure greater than 3 mm Hg (mean of 30 readings taken during each diet, p less than 0.05) while the subject was on the low salt diet. According to this definition, 16 subjects were salt-sensitive and 24 salt-resistant. During the high sodium chloride regimen, arterial pH and bicarbonate levels were significantly lower in the salt-sensitive than in the salt-resistant group (p less than 0.0001). The increase in blood pressure caused by sodium chloride correlated inversely to the arterial pH (r = -0.57, p = 0.0002) and bicarbonate levels (r = -0.52, p = 0.0007) during the high salt diet. Sodium chloride increased mean arterial blood pressure in the salt-sensitive subjects; sodium citrate did not. Sodium citrate led to an increase in pH and bicarbonate levels in both groups. Our finding that a sodium chloride-induced rise in blood pressure is associated with lower arterial plasma pH and bicarbonate levels points to an abnormality in renal acid-base regulation in salt-sensitive subjects.

Acid-Base Equilibrium↗
PubMed2000

The salt epidemic: old and new concerns.

Salt is the most suspected environmental factor which may influence arterial pressure. The recent demonstration that in the chimpanzee there is a strict dose-response relationship between salt added to food and arterial pressure and that the large majority of these animals are "salt-sensitive" is solid proof that salt has a central importance in arterial hypertension. The behavioral complexity of mankind is such that the issue of salt sensitivity is very difficult to study in man. This is probably the main reason why all attempts to validate the arterial pressure response to tests of salt sensitivity based on changes in salt intake have produced negative or inconclusive results. However our inability to reliably identify salt-sensitive individuals in no way implies that the pressor effect of salt is evenly distributed in the population or that it is intrinsically so variable that the scientific efforts aimed at defining its nature are bound to fail. We envisage that in the near future the individual "salt-sensitive risk profile" will be calculated on the basis of new scientific knowledge about hypertension genes and environmental risk factors influencing the pressor response to salt. The link between target organ damage and salt is even stronger than that between arterial pressure and salt. Left ventricular mass is closely related to salt intake. In the kidney there is evidence that high salt intake induces hyperfiltration and raises glomerular pressure. Of note the damaging potential of salt to the heart and the kidney seems to be largely independent of the ongoing arterial pressure response. A widespread reduction in salt intake at population level might in theory produce major health benefits but it seems unlikely that major public health actions will be undertaken in the near future.

Blood Pressure↗
PubMed1996

Does high salt intake cause hyperfiltration in patients with essential hypertension?

In animal models of salt-dependent hypertension, hyperfiltration is associated with a faster decline in renal function and there is evidence that in hypertensive man, increased creatinine clearance is a marker of early hypertensive nephropathy. We have studied the influence of salt intake on the glomerular filtration rate (GFR) (Creatinine Clearance) in 14 patients with mild hypertension. Each patient was studied in random order and according to a crossover design, at habitual salt intake, at high salt intake (ie habitual +50/100 mmol/day) and at low salt intake (habitual -50/100 mmol/day). Protein, calcium and potassium intake was fixed across the three study periods. The control group was formed by seven healthy subjects. High salt intake, caused a significant (P < 0.01) increase in 24 h mean arterial pressure (MAP) and the expected suppression in plasma renin activity (PRA) and in plasma aldosterone. Seven patients were classified as salt-sensitive. The GFR was significantly higher (P < 0.01) at high salt intake (125 +/- 10 ml/min) than at habitual (113 +/- 7 ml/min) and at low salt intake (97 +/- 6 ml/min). On aggregate urinary salt excretion was significantly related with the GFR (P < 0.01 by correlation analysis for repeated observations) and the slope of this relationship predicted that a 100 mmol/day increase in salt intake is associated with the 14.6 ml/min rise in the GFR. The relationship between GFR and 24 h urinary salt in salt sensitive patients did not differ from that in salt resistant patients. The GFR response to salt loading was largely independent of the renin-aldosterone system. No change in arterial pressure nor in GFR was observed in healthy subjects. At fixed protein intake, changes in salt intake in the physiological range are associated with important GFR variations in mild hypertensives. As long as hyperfiltration in mild hypertension is a predictor of renal function deterioration, high salt intake, independent of the effect of arterial pressure, could be a factor that contributes to nephronic obsolescence in patients with essential hypertension.

Adult↗
PubMed2006

Crystalline form information from multiwell plate salt screening by use of Raman microscopy.

PURPOSE: The purpose of this study was to establish a useful methodology, possibly providing information on the stoichiometry of pharmaceutical drug salts obtained from salt screening by using a multiwell plate and a Raman microscope. METHODS: Tamoxifen salt screening was conducted with monobasic and polybasic acids on 96-well quartz plates with a Raman microscope. Appearance and crystalline forms of salts prepared on 96-well plates were observed by polarizing light microscope and Raman microscope, respectively. Based on the results of the salt screening, tamoxifen citrate and fumarate salts were prepared on a large scale. The salts prepared were characterized by powder X-ray diffractometry (PXRD) and ion chromatography. RESULTS: The results of the multiwell salt screening indicated that tamoxifen has a tendency toward the formation of mono salt as opposed to hemi salt with polybasic acid, and that most of tamoxifen salts gave several potential polymorphic forms. PXRD patterns of scaled-up tamoxifen citrate and fumarate salts suggested that the same crystalline form was obtained from the binary mixture regardless of molar ratios of 2:1 or 1:1 (tamoxifen/acid). The crystalline forms obtained were tamoxifen monocitrate and monofumarate salts as measured by ion chromatography. CONCLUSIONS: Salt screening on multiwell plates with a Raman microscope provided novel insight into the characteristics prediction of the stoichiometrical salts in addition to potential polymorph information. Based on the stoichiometrical information of salts, the amount of compound and time required for crystalline form selection of drug candidates would be significantly reduced.

Chromatography, Ion Exchange↗
PubMed2005

Composition, microstructure, and surface barrier layer development during brine salting.

The goal of this study was to characterize the changes in chemical composition, porosity, and structure that occur at the surface of a block of brine-salted cheese and their relationship to the rate at which salt is taken up from the brine. To create a difference in composition, salt uptake, and barrier layer properties, identical blocks of Ragusano cheese were placed in saturated and 18% salt brine at 18 degrees C for 12 d. The overall moisture content and porosity decreased, whereas salt and salt in moisture content increased near the surface of blocks of brine-salted Ragusano cheese for all treatments. The general appearance of the microstructure of the surface of the blocks of brine-salted cheese was much more compact than the microstructure 1 mm inside the block at both brine concentrations. Large differences in porosity of the barrier layer were produced by brine-salting cheese in 18% vs. saturated brine, with cheese in saturated brine having much lower porosity at the surface and taking up much less salt during brining. The macro network of water channels within the microstructure of the cheese was less open near the surface of the block for cheese in both saturated and 18% brine after 4 d. However, no large differences in the size of the macro channels in the cheese structure due to the difference in brine concentration were observed by scanning electron microscopy. It is possible that the shrinkage of the much smaller pore structure within the casein matrix of the cheese is more important and will become more limiting to the rate of salt diffusion. Further microstructure work at higher resolution is needed to answer this question. The calculated decrease in porosity at the exterior 1-mm portion of the block was 50.8 and 29.2% for cheeses that had been in saturated vs. 18% brine for 12 d, respectively. The difference in brine concentration had a very large impact on the salt in moisture content of the cheese. The exterior of the cheese in 18% brine reached a salt in moisture content almost identical to that of the brine very quickly (17.3% at 4 d), whereas the salt in moisture content at the surface of the cheese block in saturated brine was only 11.9% at 4 d. There appears to be some critical concentration of salt in brine above which there is a large negative impact on salt uptake due to the creation of a barrier layer at the surface of the block of cheese.

Cheese↗
PubMed1996

Chlorthalidone-modulated vascular responses to vasodilator stimuli in DOCA-salt hypertensive rats.

This study was carried out to test the effect of chlorthalidone (Chlor) treatment on the vascular responsiveness to acetylcholine (Ach) and adenosine disphosphate (ADP) under different extracellular calcium concentrations (Cae2+) in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Half of the DOCA-salt hypertensive rats were simultaneously given Chlor (8 mg day-1, p.o.), after the twentieth day of DOCA, until the fortieth day. Mean arterial pressure (MAP) was reduced (P < 0.01) in DOCA-salt-Chlor (121 +/- 3 mmHg) compared to DOCA-salt (175 +/- 3 mmHg) rats. Chlor reduced the high plasma sodium of DOCA-salt to levels of the normotensive groups. The basal perfusion pressure of the isolated mesenteric vascular bed (MVB) was not modified by Cae2+ changing or previous addition of ouabain. At normal and low Cae2+ the vasodilator effect of Ach in the MVB was reduced (P < 0.01) in DOCA-salt and less (P < 0.05) in the salt-control rats. Chlor shifted the curve of DOCA-salt backward to control group curves. In high Cae2+ the vasodilator responses to Ach were reduced (P < 0.01) both in normal-control and DOCA-salt+Chlor but not in salt-control but not in salt-control and DOCA-salt group. The vasodilator effect of ADP to different Cae2+ was similar in presence of normal and low Cae2+ in normal-control rats and it was reduced (P < 0.01) in presence of high Cae2+ in the DOCA-salt group. Chlor restored the responses to ADP to normal-control level. Under ouabain-treatment, the vasodilation duration was reduced (P < 0.05) in all groups. It was shorter (P < 0.01) in DOCA-salt than in the other ones. Chlor completely abolished this difference. The MAP reduction in DOCA-salt rats by chlor could also be associated with a restored normal responsiveness of endothelial cells to endogenous vasodilator, for example Ach and ADP, since sodium nitroprusside did not exhibit differences among the various treatments. This diuretic agent seems to elicit its effect through a reduction in plasma sodium content of DOCA-salt hypertensive rats.

Animals↗
PubMed2004

A major QTL conditioning salt tolerance in S-100 soybean and descendent cultivars.

Deployment of salt tolerant cultivars is an effective approach to minimize yield loss in a saline soil. In soybean, Glycine max (L.) Merr., substantial genetic variation exists for salt response. However, breeding for salt tolerance is hampered because no economically viable screening method has been developed for practical breeding. To facilitate the development of an effective screening method for salt tolerance in soybean, the present study was conducted to determine the heritability of salt tolerance and to identify associated quantitative trait loci (QTL). F2:5 lines from the cross of 'S-100' (salt tolerant) x 'Tokyo' (salt sensitive) were evaluated in a saline field in Hyde County, N.C., USA, in 1999 and in a greenhouse located in Raleigh, N.C., USA, in 2001. S-100 and Tokyo are ancestors of popular soybean cultivars released for the southern USA. The visual salt tolerance ratings of the F2:5 lines ranged from 0 (complete death) to 5 (normal healthy appearance). The entry-mean heritability for salt tolerance was 0.85, 0.48, and 0.57 in the field (four replications), greenhouse (two replications), and combined environments, respectively. The genotypic correlation between field and greenhouse ratings was 0.55, indicating reasonably good agreement between the two screening environments. To identify QTL associated with salt tolerance, each line was characterized with RFLP markers and an initial QTL single-factor analysis was completed. These results were used to identify genomic regions associated with the trait and to saturate the selected genomic regions with SSR markers to improve mapping precision. Subsequently, a major QTL for salt tolerance was discovered near the Sat_091 SSR marker on linkage group (LG) N, accounting for 41, 60, and 79% of the total genetic variation for salt tolerance in the field, greenhouse, and combined environments, respectively. The QTL allele associated with tolerance was derived from S-100. Pedigree tracking was used to examine the association between the salt tolerance QTL and flanking SSR marker alleles in U.S. cultivars descended from S-100 or Tokyo through 60 years of breeding. The presence of alleles from S-100 at the Sat_091 and Satt237 marker loci was always associated with salt tolerance in descendants. Alleles from Tokyo for these same markers were generally associated with salt sensitivity in descendent cultivars. The strong relationship between the SSR marker alleles and salt tolerance suggests that these markers could be used for marker-assisted selection in commercial breeding.

Adaptation, Physiological↗
PubMed1988

The spontaneously hypertensive rat's preference for salted foods.

Sprague-Dawley rats drink mild salt (NaCl) solutions in preference to plain water. In contrast, rats of this strain are less likely to show preferences when salt is tested in food. Others have established that rats of the spontaneously hypertensive strain (SHR) have greater preferences for salt water than do their normotensive counterparts (WKY). The question addressed in the present research was whether SHR rats would show an enhanced salted food preference when compared with WKY rats. SHR and WKY rats were given choices between a variety of salted and unsalted foods. When tested with potato chips, no major strain differences in salt preferences were observed; depending on concentrations, rats ate either equal amounts of salted and unsalted chips or avoided salted chips. However, when tested with liquid milk products (heavy cream and half & half), SHR rats showed both higher salt preferences and consumed more salt. The SHR actually preferred these products salted, whereas the WKY rats, like Sprague-Dawley rats, never ate more salted milk than plain milk. When tested with skim milk, SHR and WKY did not differ; both preferred the milk salted. In order to test the effect of physical state (or texture) upon salt preference, the skim milk was gelled. Salt preferences of the SHR rats fell to 50% whereas the salt preferences of the WKY rats remained unchanged.

Animals↗
PubMed1999

Reduced sympathetic inhibition in salt-sensitive Japanese young adults.

The purpose of our study was to investigate the sympathetic response to excess salt loading of 54 normotensive young adults with and without a family history of hypertension. We examined muscle sympathetic nerve activity, plasma concentration and urinary excretion of catecholamines, and ambulatory blood pressures during low (4 g NaCl) and high (16 g NaCl) salt diet intake. Ambulatory blood pressure and urinary excretion of catecholamines are known to be reduced during sleep. These parameters were therefore calculated during waking and sleeping periods. The subject was defined as salt-sensitive when mean ambulatory systolic pressure during the waking period was > or =3 mm Hg higher during high salt intake than during low salt intake (n = 26: 21.4+/-0.3 years old). When mean systolic pressure was either lower or equal during high salt intake than during low salt intake, the subject was defined as salt-resistant (n = 24: 21.3+/-0.3 years old). Muscle sympathetic nerve activity, plasma concentration and urinary excretion of norepinephrine in salt-resistant subjects were significantly reduced (P<.05) by salt intake, whereas plasma concentration of epinephrine was unchanged and urinary excretion of epinephrine was reduced. In contrast, urinary excretion of epinephrine in salt-sensitive subjects was significantly elevated (P<.05) during high salt intake, whereas muscle sympathetic nerve activity and urinary excretion of norepinephrine remained unchanged despite a significant increase (P<.01) of ambulatory blood pressure. Of the salt-sensitive subjects, 73% (19 of 26) had a positive family history of hypertension, whereas only 5 of 24 salt-resistant subjects had a positive family history. These data indicate that the inhibition of sympathetic activity during a high salt intake did not occur in salt-sensitive young adults, and this may be linked with a hereditary predisposition to hypertension.

Adult↗
PubMed1988

Sodium depletion increases rats' preferences for salted food.

In contrast to humans, sodium-replete rats prefer dilute saline to water and do not prefer salted food to plain food. Sodium depletion is known to enhance the intake of and preference for salt provided in water. Here, we examined whether the context of the delivery vehicle for salt could influence salt intake and preference. This was done by studying the effects of sodium depletion on rats' preferences for salted food and salt water. In Experiment 1, rats were depleted of sodium by combined use of a sodium-deficient diet and administration of the natriuretic drug, furosemide (5 mg sc). They were then given a choice between either salted sodium-deficient diet (1% NaCl) and unsalted sodium-deficient diet or salt water (0.3 M NaCl) and water. The rats consumed more salted than unsalted sodium-deficient diet and more 0.3 M NaCl than water. However, the amount of salt ingested in food was substantially less than the amount in water. In Experiments 2 and 3 we examined preferences for various concentrations of salt (0.06%-8.0% NaCl) in food during sodium depletion. The duration of the salted food preference was inversely related to the quantity of salt consumed and the concentration of salt in the food. Data from Experiments 4 and 5 indicated that it was unlikely the changes in salted food preference were the result of taste aversions produced by furosemide administration. Taken together, these experiments demonstrate that, as the case for fluids, a preference for salted food can be produced by sodium depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗