Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SALTS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1990

Patch clamp studies on root cell vacuoles of a salt-tolerant and a salt-sensitive plantago species : regulation of channel activity by salt stress.

Plantago media L. and Plantago maritima L. differ in their strategy toward salt stress, a major difference being the uptake and distribution of ions. Patch clamp techniques were applied to root cell vacuoles to study the tonoplast channel characteristics. In both species the major channel found was a 60 to 70 picosiemens channel with a low ion selectivity. The conductance of this channel for Na(+) was the same as for K(+), P(K) (+)/P(Na) (+) = 1, whereas the cation/anion selectivity (P(K) (+)/P(c1) (-)) was about 5. Gating characteristics were voltage and calcium dependent. An additional smaller channel of 25 picosiemens was present in P. maritima. In the whole vacuole configuration, the summation of the single channel currents resulted in slowly activated inward currents (t((1/2)) = 1.2 second). Inwardly directed, ATP-dependent currents could be measured against a DeltapH gradient of 1.5 units over the tonoplast. This observation strongly indicated the physiological intactness of the used vacuoles. The open probability of the tonoplast channels dramatically decreased when plants were grown on NaCl, although single channel conductance and selectivity were not altered.

Journal Article↗
PubMed2000

Salt fortified with diethylcarbamazine (DEC) as an effective intervention for lymphatic filariasis, with lessons learned from salt iodization programmes.

DEC-fortified salt has been used successfully as a principal public health tool to eliminate lymphatic filariasis (LF) in China and, less extensively, in several other countries. Studies from 1967 to the present conducted in Brazil, Japan, Tanzania, India, China, and Taiwan involving administration of DEC salt for 18 days to 1 year, have shown this intervention to be effective for both bancroftian and brugian filariasis, as measured by reductions in both microfilarial density and positivity, and in some studies through reduction in mosquito positivity rates as well. Furthermore, studies suggest specific advantages from using DEC salt, including lack of side effects, particularly for bancroftian filariasis, and ability to reduce prevalence below 1% when used in conjunction with standard regimens of DEC tablets. However, use of DEC salt as a control tool suffers from a concern that health authorities might find it difficult to manage a programme involving a commodity such as salt. In the past decade, the very successful global efforts to eliminate iodine deficiency through universal salt iodization have demonstrated that partnership with the salt industry can be both successful and effective as a public health tool. Use of DEC salt can be most successfully implemented in areas in which (a) there is adequate governmental support for its use and for elimination of filariasis, (b) filariasis-endemic areas are clearly defined, (c) political leaders, health officials and the salt industry agree that DEC salt is an appropriate intervention, (d) the salt industry is well-organized and has known distribution patterns, (e) a successful national salt iodization effort exists, (f) a monitoring system exists that ensures adequacy of salt iodine content during production and that can also measure household coverage, and (g) measurement of impact on transmission of LF with the new antigen or filarial DNA detection methods can be established. There are advantages and disadvantages of using DEC-fortified salt compared with other interventions for LF elimination programmes, but rather than being considered as a 'competing' intervention, DEC salt should be seen as an additional option. Indeed, it is likely that many countries will derive maximal benefit from the synergistic effects of combining different intervention strategies in their national programmes to eliminate lymphatic filariasis.

Diethylcarbamazine↗
PubMed2006

Effect of salt on isoprostanes in salt-sensitive essential hypertension.

The controversy over beneficial versus harmful effects of salt on cardiovascular outcomes may be caused by different effects of salt on intermediate phenotypes of hypertension not characterized in epidemiological studies. Hence, we investigated acute effects of salt on oxidative stress in hypertensive subjects classified as salt sensitive (SS, n=14) or salt resistant (SR, n=13) by an inpatient protocol of salt loading (460 mmol NaCl) and salt depletion (10 mmol NaCl and furosemide). Oxidative stress was assessed by measuring the plasma isoprostane 8-iso-PGF2alpha. SS had lower plasma renin activity, higher aldosterone/renin ratios, and exaggerated endothelin and catecholamine responses to salt depletion compared with SR. Baseline lipid-bound isoprostanes (749+/-70 pmol/L) were 83% of the total and were slightly but not significantly higher in SS than SR. Baseline free isoprostanes did not differ between groups. After salt loading, lipid-bound isoprostanes were higher in SS (945+/-106) than SR (579+/-57; P<0.01). Salt depletion significantly decreased them in SS (-174+/-84) and increased them in SR (+129+/-58), equalizing their levels (771+/-61 versus 708+/-91; P value not significant). Free isoprostanes were decreased by salt depletion only if data in all of the patients were analyzed together. Total isoprostanes followed the pattern of the lipid-bound fraction. Correlations between salt depletion-induced changes in lipid-bound isoprostanes, plasma renin activity (r=0.45; P<0.02), and aldosterone/renin ratios (r=-0.41; P<0.04) suggested that the more SS the patient, the greater the reduction of oxidative stress by salt depletion. Our research is the first to show that salt affects oxidative stress acutely in humans, particularly in SS hypertension, which may explain the controversial results of epidemiological studies on salt and morbidity and may have implications for therapy.

Adult↗
PubMed2004

Relationship between the awareness of salt restriction and the actual salt intake in hypertensive patients.

A 24-h home urine collection was conducted to estimate accurate salt intake in hypertensive outpatients. Using 24-h urinary creatinine excretion as a criterion for success, urine samples were obtained from 534 hypertensive patients. The urinary salt excretion of hypertensive outpatients ranged widely from 1.5 to 23.4 g/day (mean value 9.7 +/- 3.9 g/day). Urinary salt excretion was higher in males than in females (10.6 +/- 4.0 vs. 9.2 +/- 3.7 g/day, p<0.01). Based on the questionnaires, the patients were divided into salt-conscious patients, or those who were careful to reduce their daily salt intake, and non-salt-conscious patients. It was found that urinary salt excretion was lower in the salt-conscious group than in the non-salt-conscious group (9.4 +/- 3.8 vs. 10.6 +/- 4.0 g/day, p<0.01), but that urinary salt excretion adjusted for body weight was not significantly different between the two groups (0.16 +/- 0.06 vs. 0.17 +/- 0.07 g/kg/day). Our results suggest that there was no obvious reduction in the actual salt intake in salt-conscious patients, suggesting the importance of monitoring salt intake by 24-h home urine collection and informing patients of their actual salt intake as a means of encouraging the achievement of salt restriction.

Aged↗
PubMed1988

NTP Toxicology and Carcinogenesis Studies of Malonaldehyde, Sodium Salt (3-Hydroxy-2-propenal, Sodium Salt) (CAS No. 24382-04-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Malonaldehyde occurs as a natural metabolic byproduct of prostaglandin biosynthesis and as an end product of polyunsaturated lipid peroxidation. Toxicology and carcinogenesis studies of malonaldehyde were conducted by administering the chemical as malonaldehyde, sodium salt, a stabilized form of malonaldehyde, in distilled water by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, and two years. The study material was 63%-79% malonaldehyde, sodium salt, 22%-38% water, and 1% or less other impurities. The water content was taken into account when the dose mixtures were prepared. Fourteen-Day and Thirteen-Week Studies: In the 14-day studies, groups of five rats and five mice of each sex were dosed with 250, 500, 750, 1,000, or 1,500 mg/kg malonaldehyde, sodium salt. Controls were untreated. Rats and mice that received 1,500 mg/kg malonaldehyde, sodium salt, did not survive to the end of the 14-day studies. No compound-related gross lesions were seen in the dosed animals. In the 13-week studies, groups of 10 males and 10 females of each species were administered 0, 30, 60, 125, 250, or 500 mg/kg malonaldehyde, sodium salt. Nine of 10 male rats, 10/10 female rats, 3/10 male mice, and 1/10 female mice that received 500 mg/kg malonaldehyde, sodium salt, died before the end of the studies. Body weights were reduced by more than 15% in rats receiving 250 or 500 mg/kg and in mice receiving 500 mg/kg. Compound-related nonneoplastic lesions were present in the stomach, testis, and kidney of rats and in the pancreas, stomach, and testis of mice. Focal and multifocal erosive lesions were observed in the gastric mucosa of the glandular stomach in the 500 mg/kg groups of male and female rats. Dilatation of the gastric glands of the stomach mucosa occurred in the 500 mg/kg male mice. Lesions of the kidney included membranous glomerular nephropathy in the 250 and 500 mg/kg male rats and the 125, 250, and 500 mg/kg female rats and mineralization in the 250 and 500 mg/kg male rats and the 60, 125, 250, and 500 mg/kg female rats. Degeneration of the testicular germinal epithelium was observed in male rats and male mice receiving 250 and 500 mg/kg. Atrophy of the exocrine pancreas was seen in the 125, 250, and 500 mg/kg male and the 250 and 500 mg/kg female mice. Based on these results, 2-year studies of malonaldehyde, sodium salt, were conducted by exposing groups of 50F344/N rats of each sex at doses of 0, 50, or 100 mg/kg, administered 5 days per week for 103 weeks. Doses of 0, 60, or 120 mg/kg were administered in the same schedule to groups of 50 male and 50 female B6C3F1 mice. Body Weight and Survival in the Two-Year Studies: Final mean body weights at the end of the study were reduced by 26% and 36% for high dose male and female rats compared with those for the vehicle controls. The final mean body weight of high dose male mice was 92% that of the vehicle controls. The final mean body weights of low dose male mice, low dose rats, and all groups of female mice were comparable to those of the vehicle controls. The survival of high dose male and female rats was significantly lower than that of the vehicle controls, with survival declining rapidly after week 76 for high dose males and after week 59 for high dose females (survival-- male: vehicle control, 37/50; low dose, 33/50; high dose, 15/50; female: 37/50; 37/50; 14/50). Survival of all groups of male mice was low (male: 24/50; 20/50; 14/50; female: 41/50; 38/50; 30/50). Survival of the high dose groups of male mice was significantly lower than that of the vehicle controls; no other significant differences in survival were observed between any groups of mice. Nonneoplastic and Neoplastic Effects in the Two-Year Studies: The incidences of a variety of nonneoplastic lesions were increased in dosed rats of each sex, primarily in the high dose male and female rat groups. These lesions were ulceration and inflammation of the glandular stomach; epithelial hyperplasia of the forestomach; inflammation of the cornea, retinal atrophy, and cataracts of the crysttion of the cornea, retinal atrophy, and cataracts of the crystalline lens; focal lipoid degeneration of the adrenal cortex; and diffuse pancreatic atrophy. Cytoplasmic vacuolization and cystic degeneration in the liver occurred at increased incidences in the high dose rat groups; in addition, the incidences of bile duct hyperplasia and bile duct fibrosis were increased in the high dose female and male rat groups, respectively. Bone marrow hematopoietic hyperplasia, hematopoiesis of the spleen, and ultimobranchial cysts of thyroid gland occurred with increased incidences in high dose female rats. The incidences of thyroid gland follicular cell adenomas or carcinomas (combined) were significantly increased in high dose male (vehicle control, 4/50; low dose, 8/49; high dose, 13/50) and female (2/50; 1/50; 7/50) rats. Follicular cell hyperplasia of the thyroid gland also occurred at an increased incidence in high dose female rats (10/50; 10/50;26/50) but not in male rats (9/50; 7/49; 7/50). The incidence of pancreatic islet cell adenomas was increased in low dose male rats (0/49; 9/50; 1/49). Adenomas and adenomas or carcinomas (combined) of the anterior pituitary gland occurred at significantly lower incidences in high dose rats than those in vehicle controls (combined incidence--male: 20/47; 14/49; 8/49; female: 18/49; 10/49; 2/48). Nonneoplastic lesions that occurred at increased incidences in dosed mice included atrophy of the pancreatic acinus and dilatation of the uterus. Depigmentation of hair shafts and change of coat color from agouti to gray were observed in high dose mice. No compound-related neoplasms were observed in dosed mice. Genetic Toxicology: Malonaldehyde, sodium salt, was not mutagenic in the Salmonella typhimurium/microsome assay when tested at doses of up to 10,000 ug/plate in a preincubational protocol using the excision-repair deficient strains TA98, TA100, TA1535, and TA1537 with or without S9 metabolic activation. The chemical induced forward mutations in mouse L5178Y lymphoma cells in the absence of S9; it was not tested with S9. Malonaldehyde, sodium salt was not mutagenic in the Drosophila melanogaster sex-linked recessive lethal mutagenicity test in which adult male flies were exposed either by feeding or by abdominal injection. In cytogenetic assays with cultured Chinese hamster ovary (CHO) cells, malonaldehyde, sodium salt, produced a dose-related increase in the frequency of sister-chromatid exchanges both in the presence and absence of rat liver S9; no increase in the number of chromosomal aberrations was observed in CHO cells in the absence or presence of S9. Audit: The data, documents, and pathology materials from the 2-year studies of malonaldehyde, sodium salt, have been audited. The audit found no special circumstances or significant deficiencies in the conduct or documentation of the studies which needed to be taken into consideration for reporting purposes. Conclusions: Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity for male and female F344/N rats administered malonaldehyde, sodium salt, as shown by the increased incidences of follicular cell adenomas or carcinomas (combined) of the thyroid gland. Pancreatic islet cell adenomas were also observed at an increased incidence in low dose male rats. There was no evidence of carcinogenic activity for B6C3F1 mice administered 60 or 120 mg/kg malonaldehyde, sodium salt, in distilled water by gavage 5 days per week for 2 years. Chemically related increased incidences of nonneoplastic lesions included ulcers and inflammation of the glandular stomach and epithelial hyperplasia of the forestomach; corneal inflammation, retinal atrophy, and cataracts of the crystalline lens; and cystic degeneration of the liver, bile duct fibrosis, and bile duct hyperplasia in rats. Most of these nonneoplastic lesions as well as the thyroid gland follicular cell neoplasms occurred primarily in the high dose rat groups, in which survival and final body weights were reduced in high dose male and female rats. Increased incidences of atrophy of the pancreatic acinus and pigmentation loss in hair shafts were seen in high dose mice. Synonyms: malonaldehyde, enol, sodium salt; propanedial, sodium; 3-hydroxy-2-propenal, sodium salt; sodium b-oxyacrolein

Journal Article↗
PubMed1994

Bile salt-dependent and bile salt-independent cholesteryl ester hydrolase activities in rat liver cytosol.

These studies report on the relationship between the bile salt-dependent and -independent cholesteryl ester hydrolase (CEH) activities found in rat liver cytosol. The two activities show very similar Michaelis-Menten substrate kinetics and pH dependence. After gel filtration of cytosol, the bile salt-independent activity elutes much earlier than the bile salt-dependent activity, suggesting that the two activities are associated with entities of different molecular size. However, when gel filtration is carried out in the presence of bile salt, the bile salt-dependent activity elutes as a large aggregate, similar to the bile salt-independent activity's behavior in the absence of bile salt. Both activities coelute after cytosol is passed through an ion exchange column. After each chromatographic procedure the recovery of the bile salt-dependent activity was substantially higher than the recovery of the bile salt-independent activity. When cytosol is incubated with anti-rat pancreatic CEH in the absence of cholate, the bile salt-dependent activity is inhibited more than 90% whereas bile salt-independent activity remains unaffected even at high antibody concentrations. When cytosol is incubated with anti-rat pancreatic CEH in the presence of cholate both CEH activities remain unaffected. The prevention of immunoinhibition by cholate seems to be specific for this detergent since CHAPS, a cholate analog, does not prevent immunoinhibition of the bile salt-dependent activity by anti-CEH. The experimental results are consistent with a model for CEH activity in liver cytosol in which there is only one enzyme that can exist in a monomeric, inactive form (that can be activated by addition of cholate to the assay and represents the bile salt-dependent activity) and in an active complex comprising several enzyme monomers as well as cholate micelles (that accounts for the bile salt-independent activity).

Animals↗
PubMed1989

Limited compensation by table salt for reduced salt within a meal.

Sixteen subjects, all of whom had said in a preliminary questionnaire that they normally added table salt to foods, were fed standard meals in the laboratory over 10 days. The meals were identical, except that on 5 days the meal had no added salt (containing 0.46 g sodium chloride) or had salt added to a level of 5.09 g. They were allowed free access to salt pots with the meals and used an average of 1.40 g table salt with the unsalted meal and 0.36 g with the salted meal, thus compensating for 22% of the difference in salt content of the meal. There was no difference in water consumption between the two types of meal. Nutrient intake from the rest of the diet did not differ between periods with high and low salt meals. The failure to compensate more fully for reduced salt in the foods can be attributed to the greater availability of table salt for perception; less table salt than salt incorporated in the foods is therefore required. Reduction of salt concentrations in purchased foods would be unlikely to be fully replaced by the consumer adding table salt.

Analysis of Variance↗
PubMed2000

Effects of isradipine or enalapril on blood pressure in salt-sensitive hypertensives during low and high dietary salt intake. MIST II Trial Investigators.

This large multicenter study, tested the antihypertensive effects of isradipine, a dihydropyridine calcium channel blocker and enalapril, an angiotensin-converting enzyme inhibitor, in salt-sensitive hypertensive patients under low and high salt intake diets. After a 3-week (weeks -9 to -6) of ad lib salt diet, those patients who had a sitting diastolic blood pressure (SDBP) of > or =95 but < or =115 mm Hg qualified to enter a 3-week (weeks -6 to -3) placebo run-in low salt diet (50 to 80 mmol Na+/day). Then high salt (200 to 250 mmol Na+/day) was added to the placebo treatment for 3 weeks (weeks -3 to 0). Those patients who demonstrated an increase in SDBP > or =5 mm Hg from the low to high salt diet were considered salt sensitive and were randomized into a 4-week (weeks 0 to 4) double-blind treatment period of either isradipine 2.5 to 10 mg twice a day, enalapril 2.5 to 20 mg twice a day, or placebo. Then they entered a 3-week (weeks 4 to 7) placebo washout phase of low salt diet (50 to 80 mmol Na+/day). After week 7 and while the low salt diet was continued the patients were restarted on their double-blind treatment for 4 more weeks (weeks 7 to 11) and the study was completed. Of 1,916 patients screened, 464 were randomized into the double-blind treatment phase and 397 completed the study. Both isradipine and enalapril decreased the sitting systolic blood pressure (SSBP) and SDBP during the high salt diet, to a similar degree, whereas enalapril caused a greater reduction in SSBP and SDBP than isradipine during the low salt diet (11.3 +/- 1.2/7.7 +/- 0.7 mm Hg v 7.7 +/- 0.9/4.8 +/- 0.6 mm Hg, mean +/- SEM, respectively, P < .02). Within drugs, the effect of isradipine on blood pressure (BP) was higher during the high than the low salt diet (14.9 +/- 1.5 v 7.6 +/- 1.3 mm Hg for SSBP and 10.1 +/- 0.6 v 4.8 +/- 0.9 mm Hg for SDBP, P < .001), but enalapril exerted a similar effect during both diets. Because salt restriction lowered both SSBP and SDBP, the lowest BP achieved with both drugs were during the salt restriction phase.

Age Factors↗
PubMed1999

Ambulatory blood pressure nondipping status in salt-sensitive and salt-resistant black adolescents.

This study examined the relationship between salt sensitivity and ambulatory blood pressure in 53 healthy black adolescents. Salt sensitivity was defined as an increase in mean blood pressure greater than or exceeding 5 mm Hg from a 5-day low-salt diet (50 mmol/24 h) to a 10-day high-salt diet (150 mmol/24 h NaCl supplement). Sixteen subjects were salt sensitive and 37 subjects were salt resistant (showed < 5 mm Hg increase in mean blood pressure). Subjects were classified as dippers (> or =10% decrease in blood pressure from awake to asleep) based on their 24-h ambulatory blood pressure values. Nondippers showed higher systolic, diastolic, and mean asleep blood pressures than dippers (P < .05 for all). Salt-sensitive subjects showed greater daytime diastolic and mean blood pressures than salt-resistant subjects (P < .05 for both). A significantly greater percentage of nondippers were salt sensitive, compared with salt resistant for diastolic blood pressure (P < .001) and mean blood pressure (P < .05). For both of these blood pressure measures, 50% of the salt-sensitive subjects had a nondipping status, compared with only 5.4% of the salt-resistant subjects for diastolic blood pressure, and 18.9% of the salt-resistant subjects for mean blood pressure. These results are the first to indicate that salt sensitivity is associated with nondipper blood pressure status in a black normotensive adolescent population.

Adolescent↗
PubMed1988

Blood pressure, salt appetite and mortality of genetically hypertensive and normotensive rats maintained on high and low salt diets from weaning.

1. Blood pressure, bodyweight, saline preference and mortality rate were examined in spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive control Wistar-Kyoto (WKY) rats maintained on low (0.1% NaCl w/w), control (0.8% w/w) and high (3% w/w) salt diets from weaning until 6 months of age. 2. The growth rate of SHR on high salt diet was not significantly different from that on control diet but SHR maintained on a low salt diet exhibited a markedly reduced growth rate. While the growth rate of WKY on low salt diet was not significantly different from that on control diet, the bodyweights of WKY on high salt diet were significantly greater than those of animals on control diet. 3. While low salt diet markedly attenuated the development of hypertension in the SHR, high salt diet significantly exacerbated the blood pressure of this strain. Neither high nor low salt diet altered the blood pressure of WKY. 4. SHR on high and low salt diets had an increased mortality rate compared with SHR on control salt diet but these differences were of slight statistical significance. Conversely, WKY on all three diets exhibited similar mortalities over the 6-month observation period. There were no significant differences in mortalities between SHR and WKY on any diet. 5. The preference for 0.9% saline, when offered as a choice with water, was not significantly different between SHR on the different diets. WKY on high salt diet, however, exhibited a significantly reduced preference for saline over the 10-day test period compared with animals on control or low salt diet. 6. Thus dietary salt modulates the hypertension of SHR but not the blood pressure of WKY. SHR would appear to require more dietary sodium for normal growth and perhaps full expression of its hypertension. The higher and lower blood pressures of the SHR on high and low salt diet, respectively, were associated with increased mortality, which was a trend not seen in the WKY.

Animals↗
PubMed2001

Regulation of plasma endothelin by salt in salt-sensitive hypertension.

BACKGROUND: Salt dependency of blood pressure (BP) characterizes most models of experimental hypertension in which endothelins play a significant vasoconstrictor role. Despite this, there are no data on the regulation of plasma endothelin by salt balance in human hypertension. METHODS AND RESULTS: Plasma endothelin was measured in 47 patients with essential hypertension. Endothelin, catecholamine, and plasma renin activity (PRA) responses to 24-hour sodium deprivation (decreasing Na) were assessed in 29 of these patients. Endothelin was higher in hypertensive patients (4.6+/-0.2 fmol/mL) than in 20 control subjects (3.3+/-0.3 fmol/mL, P:<0.002), was correlated with BP, and was negatively associated with PRA (P:<0.04). Salt-sensitive, salt-resistant, and indeterminate groups were defined by the tertiles of the t statistic for the difference in BP before and after decreasing Na. Systolic BP falls were -15+/-1, -2+/-2, and -9+/-1 mm Hg, respectively. PRA, its response to decreasing Na, and its level after decreasing Na were lowest (albeit nonsignificant) in salt-sensitive patients. Baseline catecholamine and endothelin levels did not differ among the groups. In response to decreasing Na, catecholamines increased more significantly in salt-sensitive patients (+2.4+/-0.9 nmol/L) than in the other groups (0.4+/-0.2 and 0.7+/-0.2 nmol/L for indeterminate and salt-resistant groups, respectively; P:<0.03), whereas endothelin increased in the salt-sensitive group (0.8+/-0.3 fmol/mL), decreased in the salt-resistant group (-0.4+/-0.3 fmol/mL), and sustained minimal change in the indeterminate group (0.2+/-0.3 fmol/mL) (P:<0.04). Thus, endothelin levels in the salt-depleted state were highest in salt-sensitive patients (5.2+/-0.4 fmol/mL) versus the other groups (3.4+/-0.4 and 4.4+/-0.4 fmol/mL for salt-resistant and indeterminate groups, respectively) (P:<0.02). Changes in endothelin during decreasing Na and levels after decreasing Na were correlated with changes in catecholamines (P:<0.02). CONCLUSIONS: -Our data suggest that salt-depleted salt-sensitive hypertensives with blunted renin responses exhibit enhanced catecholamine-stimulated endothelin levels and may therefore respond better than unselected patients with essential hypertension to endothelin receptor blockers.

Blood Pressure↗
PubMed1987

Sensitization of aortic baroreceptors by high salt diet in Dahl salt-resistant rats.

High salt diet alters neural cardiovascular control. This influence has been attributed to central neural or efferent mechanisms. To test the hypothesis that a high salt diet might alter afferent baroreceptor function, Dahl salt-resistant (DR) and salt-sensitive rats (DS) were fed a high or a low salt diet. Blood pressure was measured intra-arterially in unanesthetized animals. Aortic baroreceptor function was then evaluated during urethane anesthesia by recording multifiber aortic depressor nerve activity during a phenylephrine-induced blood pressure ramp. Mean arterial pressure in the conscious state was elevated (155 +/- 5 [SE]mm Hg) in DS fed a high salt diet but was normal in DS fed a low salt diet and in DR. Slopes of linear regressions relating aortic nerve discharge to mean arterial pressure were 71% higher in DR fed a high salt diet than in DR fed a low salt diet (p less than 0.025), indicating that high salt potentiated baroreceptor function in DR. In contrast, high salt diet produced no significant effects on baroreceptor function in DS. No salt-induced changes in dynamic or static aortic distensibility (assessed from pressure-volume curves of the in situ isolated arch) were detectable in either rat strain. Absence of salt-induced baroreceptor sensitization in DS was not due to the hypertensive state because the sensitization also failed to occur in separate groups of DS in which salt-induced hypertension had been prevented by chemical sympathectomy with 6-OH-dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Nitric oxide synthase and renin-angiotensin system gene expression in salt-sensitive and salt-resistant Sabra rats.

The molecular mechanisms of salt sensitivity and the contribution of the kidney to salt-induced hypertension in Sabra rats are imperfectly defined. We investigated the expression of the nitric oxide (NO) system (endothelial, inducible, and neural NO synthases) and renin-angiotensin system (renin, angiotensinogen, and angiotensin II type 1A receptor) gene components in the kidneys of SBN/y (salt-resistant) and SBH/y (salt-sensitive) Sabra rat substrains, with and without deoxycorticosterone acetate (DOCA)-salt treatment. We also looked for immunocytochemical evidence of angiotensin II, the effector peptide of the renin-angiotensin system. Inducible and neural NO synthase gene expression values were lower in SBH/y than in SBN/y before and after DOCA-salt treatment. The gene expression level of endothelial NO synthase was not different in SBH/y and SBN/y, either with or without DOCA salt. Renin gene expression was significantly higher in kidneys of SBN/y than in kidneys of SBH/y rats, whereas angiotensinogen gene expression was significantly lower in SBN/y. After DOCA-salt treatment, renin gene expression was strongly suppressed in both strains but more so in SBH/y. Angiotensinogen gene expression, on the other hand, was increased by DOCA salt in SBN/y rats so that the two strains were no longer different. Angiotensin II immunoreactivity was significantly higher in SBN/y than in SBH/y; however, after DOCA salt, immunoreactivity in both strains was no longer detectable. Angiotensin II type 1A receptor gene expression was not different between the two strains, either before or after DOCA-salt administration. We conclude that DOCA salt induced a decrease in the activity of the renin-angiotensin system but did not change NO synthase gene expression in SBH/y and SBN/y. Inducible and neural NO synthase gene expression values were less in SBH/y than in SBN/y, independent of DOCA-salt administration. Thus, the NO system could explain, at least in part, the salt resistance of SBN/y.

Angiotensin II↗
PubMedDate not supplied

[Hormonal profile and participation of nitric oxide in salt-sensitive and salt-resistant essential arterial hypertension].

Recent studies have shown that cardiovascular events and end-organ damage occur more frequently in patients with salt-sensitive essential hypertension (SH) than in salt-resistant essential hypertension (RH). Nitric oxide (NO) plays an important role in regulating the pressure-natriuresis relationship. Therefore impaired NO synthesis may produce or aggravate salt-sensitive hypertension. This study was conducted to determine the hormonal levels and nitric oxide metabolites in hypertensive patients. 25 patients underwent salt sensitivity testing. 24 h ambulatory blood pressure was recorded after a 5-day period on low salt diet (20 mEq/d) and after a 5-day period on a high salt diet (200 mEq/d). Subjects showing > or = 10 mmHg increase in mean BP when changing from low to high dietary salt intake were classified as salt sensitive and as salt resistant when the BP changes were < 10 mmHg. Based on BP recordings 13 patients were characterised as white coat hypertension (WC), 13 patients as salt resistant (SR) and 12 as salt sensitive (SS). A significative relationship was seen between plasma glucose-insulin concentration and body mass index. The ventricular mass index was similar in SS and SR patients. The plasma uric acid, triglicerides and PAI-I were elevated in SS compared with SR, and control group (C). During low sodium intake, plasma renin and aldosterone were decreased in SS compared with SR, and C. No differences in plasma catecholamines or their changes with intake sodium modifications were seen among the patients. During high sodium intake urinary NO excretion increased in SR (38 +/- 9 vs 18 +/- 2 mg/g creat), and C (24 +/- 2 vs 16 +/- 3 mg/g creat) (p < 0.01) but not in SS patients (21 +/- 3 vs 26 +/- 4 mg/g creat). The NO excretion changes showed negative correlation with BP changes (r = 0.49, p < 0.01). During low sodium intake, SR and SS patients showed a normal nocturnal decrease of BP (dippers). During high sodium intake SS patients became non-dippers. Our results showed that patients with salt sensitive hypertension displayed a suppressed renin-aldosterone system, an attenuated nocturnal decline in blood pressure on high-salt diet and an impairment of endothelial function. The relationship between urinary nitrate excretion and arterial pressure suggest that the salt sensitivity of arterial pressure may be related bo blunted generation of endogenous nitric oxide.

Adult↗
PubMed1995

Do changes in dietary salt influence blood pressure of hypertensive patients pharmacologically controlled with verapamil? The Salt-Switching-Study (SSS).

To study how changes in dietary salt influence the blood pressure (BP) of pharmacologically controlled hypertensive patients, we have selected from a large multicenter trial two subgroups of 14 and 16 patients who attained BP control (office DBP < 90 mm Hg) after a 4-week treatment with verapamil SR 240 mg once daily, either under an unrestricted salt diet (high-salt; 14 patients) or under a moderately restricted salt diet (low-salt; 16 patients). All of them were switched to the opposite dietary salt regimen and continued on verapamil for 4 more weeks (Salt-Switching-Period). Office BP and ambulatory blood pressure monitoring (ABPM) were registered before and after the Salt-Switching-Period. Salt intake was checked by urinary sodium excretion (UNa). Patients switching from high- to low-salt reduced UNa from 180.9 +/- 22.9 to 89 +/- 28 mM Na/24h (P < 0.001) and patients switching from low- to high-salt increased UNa from 85 +/- 38.4 to 175.8 +/- 57.5 mM Na/24h (P < 0.001). No significant changes in BP were found by ABPM either in the group switching from high- to low-salt or in the group switching from low- to high-salt. In the latter group, a significant increase was observed in office DPB but not in SBP. Short-term changes in salt intake seem to have little influence on the BP of patients pharmacologically controlled with verapamil.

Adult↗
PubMed1997

There are no racial, age, sex, or weight differences in the effect of salt on blood pressure in salt-sensitive hypertensive patients.

BACKGROUND: This report is part of a larger, multicenter, placebo-controlled study designed to test the effects of low and high salt intake on the antihypertensive action of enalapril maleate or isradipine in salt-sensitive, hypertensive patients. OBJECTIVE: To present our findings with respect to the effects of race, age, sex, and weight on the blood pressure response to low and high salt intake in salt-sensitive hypertensive patients before randomization into the larger study. PATIENTS AND METHODS: After 3 week (weeks -9 to -6) of ad lib salt intake (100-200 mmol/d of sodium), 1916 patients whose sitting diastolic blood pressure was between 95 and 115 mm Hg entered a 3-week period (week -6 to -3) of low salt intake (50-80 mmol/d of sodium) and then a 3-week period (week -3 to 0) of high salt intake (200-250 mmol/d of sodium). Of the 1916 patients, 624 were identified as being sensitive to salt by demonstrating an increase in sitting diastolic blood pressure of equal to or more than 5 mm Hg from the low to high salt intake. Of these patients, 367 were white, 156 were black, 92 were Hispanic, 8 were Asian, and 1 was American Indian. Also, 315 were men and 309, women; 351 were 55 years or younger and 273 were older than 55 years; and 195 had a body mass index of 27 or less and 429 had a body mass index higher than 27. RESULTS: The sitting blood pressure decreased with salt restriction and increased with salt load in all groups of patients (P < .001). There were no statistically significant differences in the blood pressure changes to salt changes by race, age, sex, and weight. CONCLUSIONS: This large, multicenter study did not demonstrate any statistically significant effect of race, age, sex, and weight on blood pressure response to salt changes in salt-sensitive hypertensive patients.

Aging↗
PubMed2003

Effects of microflora status, dietary bile salts and guar gum on lipid digestibility, intestinal bile salts, and histomorphology in broiler chickens.

The aim of the present study was to reexamine the effects of intestinal viscosity, microflora, and bile salts, and their interactions in order to clarify the mechanisms that explain the effect of intestinal viscosity on lipid digestibility, especially those that could involve microflora. Effects of intestinal viscosity, microflora status, and dietary bile salts on lipid digestibility, intestinal bile salts, and intestinal histomorphology were tested in a 2 x 2 x 2 factorial experiment. The effect of microflora status was examined by comparing conventional chickens to chickens with limited microflora obtained by rearing birds in sterilized conditions. Viscosity and dietary bile salts were tested with guar gum (0 or 0.5% in diets) and sodium taurocholate (0 or 0.3% in diets), respectively. Guar gum was autoclaved and added to the gamma-irradiated diets by mixing inside the sterile isolators. The intestinal concentration of lactic acid and cecal concentration of short-chain fatty acids were both very low in birds with limited microflora compared to conventional birds (P = 0.0001). Chickens with limited microflora had higher gain:feed ratios (P = 0.002), higher fecal lipid digestibility (P = 0.0001), more intestinal conjugated bile salts (P = 0.0001), less intestinal unconjugated bile salts (P = 0.0001), and their gastrointestinal compartments were smaller (P < 0.05) than those of conventional chickens. Addition of bile salts in diets increased the lipid digestibility (P = 0.0001) with a more pronounced effect in conventional birds (P = 0.0001) and in birds fed on guar gum diets (P = 0.002). Feeding the guar gum diets increased the intestinal supernatant viscosity (P = 0.0001) for both microflora status. Guar gum addition increased (P < 0.05) the lactic acid concentration in the small intestine of conventional chickens. Guar gum decreased the fecal lipid digestibility (P = 0.0001) and the intestinal conjugated bile salts (P = 0.0001) for both microflora status. However, the magnitude of lipid digestibility decrease due to guar gum was lower (P = 0.05) in birds with limited microflora than in conventional birds, and the negative effect of guar gum on intestinal conjugated bile salts was more pronounced (P = 0.02) in birds with limited microflora. Bile salt addition reduced the negative effect of guar gum on lipid digestibility (P = 0.02) for both microflora status. The mean lipid digestibilities were negatively correlated (P = 0.0001) with the ratio [Ln(viscosity)/total bile salt] measured in intestinal digesta. Except for gizzard, size of digestive compartments and villus heights increased (P < 0.05) with feed efficiency and digestibility decreased. In conclusion, the results provided evidences that the negative effect of guar gum on lipid digestibility was mainly mediated by its direct effect on intestinal bile salt concentration and efficiency. The small interaction between guar gum and microflora status effects on lipid digestibility had to be accounted for by the low basal level of intestinal bile salts in conventional chickens.

Animal Feed↗
PubMed1992

Effects of sodium salts on pressor reactivity in salt-sensitive men.

Blood pressure in patients with essential hypertension is raised by sodium chloride but not by nonchloride sodium salts. Although a high sodium chloride diet is known to augment the pressor response to norepinephrine and angiotensin II, the effect of nonchloride sodium salts on pressor responsiveness has not been studied so far. To examine whether sodium chloride and nonchloride sodium salts evoke different pressor responses to these agonists, we performed graded norepinephrine and angiotensin II infusions in salt-sensitive (n = 7) and salt-resistant (n = 8) normotensive subjects. The subjects were given a low salt diet (20 mmol/day) for 3 weeks, to which a supplement of 200 mmol sodium per day, provided as either sodium chloride or sodium citrate, or a placebo was added for 1 week each. We found that, although sodium chloride raised mean arterial blood pressure in the salt-sensitive subjects (p less than 0.005), sodium citrate did not. However, under both sodium salts pressor response to norepinephrine and angiotensin II was significantly greater than under placebo (p less than 0.02). Furthermore, with both sodium salts, pressor response in the salt-sensitive subjects was greater than in the salt-resistant subjects (p less than 0.01). This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin II. Since pressor response increased with both sodium salts but resting blood pressure increased only with sodium chloride, enhanced pressor responsiveness alone cannot account for the sodium chloride-induced rise in resting blood pressure.

Adult↗