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At least 379 records · Page 21Linked to original sources
PubMed1986

Salt or no salt in the treatment of cirrhotic ascites: a randomised study.

To compare the effect of diet, cirrhotic patients with ascites were randomised into two treatment groups: (1) a low sodium diet (21 mmol) per day or (2) an unrestricted sodium intake. Both groups received effective doses of diuretics (spironolactone or, if necessary, spironolactone and furosemide. One hundred and forty patients from 12 liver units were included according to well defined criteria (group 1: 76; group 2: 64). After an initial four to seven day period of bed rest and salt restriction (21 mmol sodium pd), randomisation was done in each centre. We saw no significant difference between the two groups with respect to clinical and biochemical data; mortality or withdrawal (definitive or temporary) because of biochemical disturbances (group 1: 34%, group 2: 22%); the time for complete disappearance of ascites was significantly shorter (p = 0.014) for the salt restricted patients actuarial survival (curves plotted up to the 120th day) was not statistically different (p = 0.18), but division into subgroups using various prognostic factors showed that survival was significantly better for salt restricted patients without previous gastrointestinal bleeding (p = 0.02); hospitalisation time and costs were identical in both groups. We conclude that the advantage of a normal salt diet was not shown in this study.

Adult↗
PubMed2000

Bile salt toxicity to some bifidobacteria strains: role of conjugated bile salt hydrolase and pH.

The purpose of this work was to study some aspects of bile salt toxicity towards bifidobacteria. A strain (Bifidobacterium coryneforme ATCC 25911) was selected for its lack of conjugated bile salt hydrolase activity (CBSH-), and was used with three deconjugating strains (CBSH+), for study of their growth and viability in the presence of two dihydroxylated conjugated bile salts (tauro- and glyco-deoxycholic acids). The presence of the glycoconjugate induced a more significant growth inhibition for the four strains than the tauroconjugate. The viability of the strains was measured at several pH levels. Glycodeoxycholic acid, but not taurodeoxycholic acid, exerted a lethal effect, which increased at low pH. This phenomenon was more pronounced for the CBSH- strain. We explain some of these results using an hypothesis based on the consequence of dissociation of conjugated and deconjugated bile salts, and the value of their pKa.

Amidohydrolases↗
PubMed1984

Differential sensitivity of Dahl salt-sensitive and Dahl salt-resistant rats to the hypotensive action of acute nifedipine administration.

The calcium antagonist, nifedipine, was intravenously administered in a cumulative fashion, from 0.5 to 12 mg/kg, to Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats which had been maintained on a high (8.0%) or low (0.4%) salt (NaCl) diet. We observed, compared with the DR rats, dose-related and significant (P less than 0.001) falls in the systolic (SBP) (72 +/- 3 and 60 +/- 9%, respectively) and diastolic blood pressure (DBP) (67 +/- 2 and 62 +/- 6%) o the DS rats maintained either on the low (0.4%) or high (8.0%) salt diets. In contrast, nifedipine therapy comparatively produced only moderate changes in the SBP and DBP of the DR rats (36 +/- 12, 27 +/- 9, 31 +/- 10, and 30 +/- 11%, respectively). We hypothesize that this differential sensitivity of the DS and DR rats to the hypotensive action of nifedipine may reflect a significantly more important role for a high resting Ca2+ influx, through nifedipine sensitive channels, in the maintenance of the blood pressure of the DS rat.

Animals↗
PubMed1993

High-salt diet upregulates activity and mRNA of renal Na(+)-K(+)-ATPase in Dahl salt-sensitive rats.

We examined the effect of a high-salt (HS) diet on the regulation of renal cortical Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) in young Dahl salt-sensitive (DS) and salt-resistant (DR) rats. The activity of Na(+)-K(+)-ATPase, determined in permeabilized proximal tubule segments, was similar in DS and DR rats on normal salt (NS) diet. HS diet resulted in a twofold increase in proximal tubule Na(+)-K(+)-ATPase activity in DS rats but not in DR rats. The mRNA abundance, which was also similar in DS and DR rats on NS diet, increased after 2 days on HS diet in both innervated and denervated kidneys from DS rats but had no effect in DR rats. The activity of Na(+)-K(+)-ATPase and the content of alpha 1- and beta-protein in cortical homogenate were similar in DS and DR rats on both NS and HS diets. Treatment with benserazide, an inhibitor of dopa decarboxylase, upregulated proximal tubule Na(+)-K(+)-ATPase activity and increased Na(+)-K(+)-ATPase mRNA in DR rats on HS diet. Taken together, these data indicate that there is a primary defect in the dynamic hormonal regulation of Na(+)-K(+)-ATPase activity in intact tubular cells, which might stimulate Na(+)-K(+)-ATPase transcription.

Animals↗
PubMed1973

Proximal and distal tubular function in salt-deprived and in salt-loaded deoxycorticosterone acetate-escaped rats.

Proximal and distal tubular function was compared with urinary excretion in rats after chronic administration of salt and deoxycorticosterone acetate (DOCA) or during salt deprivation. DOCA rats excreted significantly more sodium than did salt-deprived rats. Measurements of tubular fluid to plasma (TF/P) inulin ratios and concentrations of sodium and potassium in quantitative, timed collections, related to measured tubular length, allowed calculation of absolute reabsorption of fluid and ions in the different nephron segments. Proximal transport was not reduced in DOCA-treated rats compared with salt-deprived animals; in distal tubule the former group reabsorbed more sodium and secreted less potassium than the latter. Calculation of sodium transport in loop of Henle as the difference in flow between the end of the proximal convolution and the beginnings of the distal tubule indicated no inhibition of reabsorption in DOCA animals. Comparison of end-distal tubular flow with simultaneous urinary excretion suggested that sodium load was not the determining factor of enhanced natriuresis in DOCA-treated animals. The data are interpreted as indicating that DOCA-escape in the rat is associated with specific alteration of sodium transport in the collecting duct system.

Animals↗
PubMed1980

Effect of inhibition of converting enzyme on inactive renin in the circulation of salt-replete and salt-deplete normal subjects.

Angiotensin II exerts an inhibitory influence on active renin release from the kidney. To assess a possible role for angiotensin II in the release of inactive renin, levels in the circulation were measured before and at regular intervals after the administration of captopril, an orally active inhibitor of angiotensin I-coverting enzyme, to 12 salt-replete and six salt-deplete normal subjects. Concurrent measurements of active renin, angiotensin I and angiotensin II were also performed. Basal inactive renin in the salt-deplete group was increased compared with the salt-replete subjects, but inactive renin remained constant in both groups after treatment with captopril. There were significant increases in concentrations of both active renin and angiotensin I after treatment with captopril in all subject and corresponding decreases in angiotensin II. These results suggested that angiotensin II does not influence the release of inactive renin, in contrast with its role in the release of active renin.

Angiotensin I↗
PubMed1984

Effect of calcium phosphates and zinc in salt-mineral mixtures on ad libitum salt-mix intake and on zinc and selenium status of sheep.

In two separate experiments, 72 crossbred ewes were fed hay, haylage (50% dry matter) and corn diets with ad libitum salt-mineral mixtures (SMM; Exp. 1) or salt (Exp. 2). Calcium phosphates (Ca X P) and(or) zinc (Zn) were added in a 2 X 2 factorial arrangement to salt + trace minerals for ewes 7 mo prepartum through lactation in Exp. 1 and to salt only for ewes 3 mo prepartum through lactation in Exp. 2. The diets fed were estimated to contain 23 and 28 mg Zn/kg dry diet (ppm), respectively, and .08 and .05 ppm Se. Large variations (up to fivefold) were found in SMM intake per month between replicates and from month-to-month within treatment; thus, monthly variations of up to sevenfold occurred in Zn and Se intakes of supplemented groups. There were no significant treatment effects on SMM intake. Small but significant Zn treatment effects were detected for plasma and wool Zn of ewes and lambs, but all values were in the normal range. There was no significant treatment effect on plasma alkaline phosphatase activity. In Exp. 2, erythrocyte glutathione peroxidase (GSH-Px) activity was significantly lower in all treatment groups compared with a Se-supplemented control group but only rare occurrences of subclinical muscular dystrophy were found. There was no significant treatment effect on GSH-Px activity, whole blood Se in ewes and lambs or plasma creatine phosphokinase activity in lambs. These results indicate large animal and seasonal variability in SMM intake and no significant treatment effects of Ca X P on SMM intake or on Zn and Se status. Zinc addition to SMM had no effect on Se status.

Alkaline Phosphatase↗
PubMed2000

Increasing evidence for the role of salt and salt-sensitivity in hypertension.

The paper focuses on some aspects of the complex relationship between dietary salt intake and blood pressure. The first part is a short review of the evidence available from epidemiological and clinical studies, indicating that a moderate reduction in dietary salt intake represents an effective non-pharmacological measure for the treatment of hypertension and for the prevention of hypertension-related cardiovascular complications, namely stroke and ischemic heart disease. The second part deals with the role of inherited and acquired factors in the phenotypic expression of the salt-sensitivity of blood pressure. In particular, the influence of sympathetic nervous system hyperactivity, of insulin resistance and of alterations of endothelial function in the pathogenesis of salt-related forms of hypertension are discussed.

Age Factors↗
PubMed2003

The response of Dahl salt-sensitive and salt-resistant female rats to a space flight model.

Vitamin D metabolism in the Dahl salt-sensitive (S) rat, a model of salt-induced hypertension, differs from that in the Dahl salt-resistant (R) rat. We have tested the hypothesis that differences in vitamin D metabolism would render the Dahl S rat more susceptible than the Dahl R rat to the effects of a space flight model. Dahl female rats were tail suspended (hind limb unloaded) for 28 days, while fed a low salt (3 g/kg sodium chloride) diet. Plasma 25-OHD concentrations of S rats were significantly lower than that of R rats. Plasma 1,25-(OH)2D concentration was 50% lower in unloaded than in loaded S rats, but was unaffected in unloaded R rats. The left soleus muscle weight and breaking strength of the left femur (torsion test) were 50% and 25% lower in unloaded than in loaded S and R rats. The mineral content of the left femur, however, was significantly lower (by 11%) only in unloaded S rats. We conclude that female S rats are more vulnerable than female R rats to decreases in plasma 1,25-(OH)2D concentration and femur mineral content during hind limb unloading, but equally vulnerable to muscle atrophy and reduced breaking strength of the femur.

Animals↗
PubMed2006

Triple VPI CGS 35601 reduces high blood pressure in low-renin, high-salt Dahl salt-sensitive rats.

We previously reported that CGS 35601, a potent triple inhibitor of angiotensin-converting enzyme, neutral endopeptidase, and endothelin-converting enzyme 1, completely normalized mean arterial blood pressure (MABP) in 36-week-old spontaneously hypertensive rats, a normal renin model. The aim of the present study was to determine the effects of this triple vasopeptidase inhibitor (VPI) on the hemodynamic profile of instrumented, conscious, and unrestrained Dahl salt-sensitive (DSS) rats, a gene-prone, high-salt diet-induced low-renin hypertension model. Male DSS rats (mean weight [+/-SEM], 385 +/- 10 g) were fed a normal diet (Group 1) or a high-salt diet (Groups 2 and 3; 8% NaCl in food) for 6 weeks and then instrumented with a carotid catheter and placed individually in metabolic cages for 30 days. The hemodynamic, hematological, and biochemical profiles were assessed daily. Dose-dependent treatment started after a 7-day stabilization period in Groups 1 and 2 (vehicle dosage, 250 microl/hr) and Group 3 (CGS 35601 dosages of 0.1, 1, and 5 mg/kg/day for 6 days per dose by means of constant intra-arterial infusion), followed by a 5-day washout period. Two additional groups included normotensive Wistar rats (Group 4) and DSS rats that received a double high-salt solid (8% NaCl) and liquid (1% NaCl) diet (Group 5). The MABP in rats receiving CGS 35601 decreased in a dose-dependent fashion toward the baseline level observed in DSS rats receiving a normal diet. The heart rate was unaffected. The hemodynamic profile returned to normal during the washout period. This novel triple VPI is a potent and effective antihypertensive agent with a safe short-term profile that may be of interest for treating hypertension and other cardiovascular diseases. Other hypertensive rat models are being tested.

Animals↗
PubMed1989

Effects of oral administration of sulfolithocholic acid disodium salt and lithocholic acid sodium salt on N-methyl-N-nitrosourea-induced colonic tumorigenesis in conventional rats.

Effects of p.o. administration of sulfolithocholic acid disodium salt (SLCNa) and lithocholic acid sodium salt (LCNa) on N-methyl-N-nitrosourea (MNU)-induced colonic tumorigenesis were studied in conventional rats. Female F344 rats received either 0.5 ml of distilled water (DW) alone or DW containing 2.5 mg of MNU twice in 1 wk intrarectally. Then rats were fed freely on a basal diet (PCE-2) or PCE-2 containing LCNa or SLCNa (both at 0.5 mmol/100 g of PCE-2) for 40 wk. Thus, 6 groups were completed: MNU + PCE-2 (n = 30); MNU + LCNa (n = 29); MNU + SLCNa (n = 22); DW + PCE-2 (n = 17); DW + LCNa (n = 20); and DW + SLCNa (n = 19). Numbers of rats bearing colonic tumor were 3 (10%) in MNU + PCE-2, 2 (7%) in MNU + LCNa, and 8 (36%) in MNU + SLCNa group (uncorrected x2 = 9.35 among the 3 groups), but none in those groups without MNU. Total fecal bile acids in the rats given bile salts showed about 2-fold increase compared with those without bile salts. Fecal bile acid profiles between the LCNa and SLCNa groups were indistinguishable except for a slight increase of sulfolithocholic acid in the SLCNa groups. These results indicated that p.o. administration of SLCNa but not LCNa promoted MNU-induced colonic tumorigenesis in conventional rats. Fecal bile acid profiles did not support the higher tumor incidence in the MNU + SLCNa group compared with the MNU + LCNa group, which suggested that an unrecognized mechanism probably relating to desulfation of SLCNa was involved in this phenomenon.

Administration, Oral↗
PubMed1986

Phorbol ester receptors in cardiac myocytes of salt-sensitive and salt-resistant Dahl rats.

A moderate degree of cardiac hypertrophy develops in salt-sensitive Dahl (DS) rats after 5 weeks on a high-salt (8% NaCl) diet. Cardiac hypertrophy is accompanied by a significant reduction in the number of phorbol ester receptors on enzymatically dissociated myocytes with no changes in their affinities. In contrast, the number and properties of these receptors are not influenced by variations of dietary salt intake in the salt-resistant Dahl (DR) rat. Since phorbol esters are closely related to protein kinase C, a potent stimulator of Ca2+ transport in the heart, these results suggest that loss of phorbol ester binding sites may limit the inotropic reserve of the hypertrophied myocardium.

Animals↗
PubMed1986

Up-regulation of alpha 2 adrenoceptors and down-regulation of beta 2 adrenoceptors by high-salt diet in normotensive men: enhanced up-regulation of operative (alpha 2:beta 2) adrenoceptor ratio predicts salt sensitivity.

In 24 normotensive male volunteers (age 20-25 years) reduction of sodium intake from 200 to 50 mmol/day over 2 weeks resulted in a 14% fall of alpha 2-adrenoceptors of platelets from 209.5 to 179.4 fmol/mg (P less than 0.01) and in a 16% rise of beta 2-adrenoceptors of lymphocytes from 13.3 to 16.2 fmol/mg (P less than 0.05) which was reversible by 2 weeks of high sodium intake. In contrast to the comparatively minor changes of alpha 2- and beta 2-adrenoceptor density, the functionally probably more relevant 'operative (alpha 2:beta 2) adrenoceptor ratio' decreased by 53% from 22.9 to 14.9 (P less than 0.01) during the low-salt diet. Although neither the individual changes of alpha 2- and of beta 2-adrenoceptor densities correlated with individual blood pressure changes induced by variations in sodium intake, there was a highly significant positive correlation (r = 0.55, n = 33; P less than 0.01) between the rises of the 'operative adrenoceptor ratio' and the rises of blood pressure induced by high salt intake. We conclude that the 'operative adrenoceptor ratio', although only determined on alpha 2- and beta 2- and not on alpha 1- and beta 1-adrenoceptors, and only on circulating blood cells, may be representative for sympathetic resistance vessel tone, at least as a function of variations of salt intake. Enhanced up-regulation of the 'operative adrenoceptor ratio' in the salt-sensitive part of the population may be one important early step in the development of essential hypertension.

Adult↗
PubMed1987

Cardiac sensory receptors in Dahl salt-resistant and salt-sensitive rats.

The Dahl strain of genetically salt-resistant (DR) and salt-sensitive (DS) rats affords an opportunity to explore mechanisms responsible for salt resistance and sensitivity. Dahl sensitive rats exhibit abnormalities in sympathetic neural control of the circulation and in renal sodium handling. Since cardiac baroreflexes participate in regulation of sympathetic nerve activity and sodium excretion, we have evaluated cardiac baroreflex function in DR and DS rats. This article briefly reviews evidence that cardiac sensory endings with vagal afferents are reset to a higher threshold in DS rats before elevation of arterial or cardiac filling pressures, as a result of this resetting, cardiac baroreflex inhibition of sympathetic nerve activity during volume expansion is impaired in prehypertensive DS rats, a high-sodium diet enhances the gain of cardiac baroreflex inhibition of sympathetic nerve activity in DR but not DS rats, and atrial natriuretic factor stimulates cardiac sensory receptors with vagal afferents. Taken together, these studies prompt speculation that humoral factors released during intake of a high-sodium diet may sensitize cardiac baroreflexes and thereby protect against sodium retention and hypertension. An absence of this compensatory adjustment or plasticity in cardiac baroreflex function in DS rats may predispose to salt-induced hypertension.

Animals↗
PubMed1986

Response of the canine corneal endothelium to intraocular irrigation with saline solution, balanced salt solution, and balanced salt solution with glutathione.

The right or left anterior chamber of 12 dogs (ie, 24 eyes) was irrigated with 100 ml of 0.9% saline solution, balanced salt solution, or balanced salt solution with glutathione (8 eyes/solution) for 22 minutes. Changes in endothelial cell density and corneal thickness from pretreatment values were evaluated immediately after, and at 2 and 7 days after irrigation. Using specular microscopy and scanning and transmission electron microscopy, corneas were examined immediately after and at 2, 7, and 14 days after irrigation. Changes were not seen in endothelial cell density after irrigation with any of the solutions evaluated. Corneal thickness increased 4% immediately after irrigation with 0.9% saline solution and returned to normal by 1 week after irrigation; treatment with 0.9% saline solution was not associated with visible corneal edema. Ultrastructural changes attributable to differences in irrigating solution composition were not observed. The difference between the endothelium's response to limited irrigation with saline solution, balanced salt solution, and balanced salt solution with glutathione was small and irrigation with these solutions was not associated with permanent endothelial damage.

Acetates↗
PubMed1995

Differential distribution of alpha 2-adrenoceptor subtypes and messenger RNA expression between renal cortex of salt-sensitive and salt-resistant Sabra rats.

OBJECTIVE: To assess whether alterations of alpha 2-adrenoceptor subtypes in distribution and gene expression in the renal cortex could explain the predisposition to salt-sensitivity or salt-resistance in Sabra rats. DESIGN: Studies were performed using plasma membranes and RNA preparations from renal cortex of 8- to 10-week-old Sabra salt-sensitive (SBH) and salt-resistant (SBN) rats on a normal-sodium diet. METHODS: The alpha 2-adrenoceptor subtypes were determined by competition experiments with [3H]-yohimbine or [3H]-RX821002. Their gene expression was studied by RNA-directed complementary DNA synthesis followed by Taq DNA polymerase amplification. RESULTS: Binding studies showed that alpha 2B- and alpha 2A-adrenoceptor subtypes represented in SBN 72 and 28% of the maximal binding capacities of the two radioligands, respectively. In contrast, only the alpha 2B subtype was detected in the SBH rat. However, the use of guanoxabenz disclosed alpha 2B-adrenoceptors in alpha 2B1 and alpha 2B2 subtypes. The densities of those alpha 2B subtypes appeared to be higher in the SBH rat than in the SBN rat. Messenger RNA corresponding to alpha 2A and alpha 2B subtypes were found both in SBH rats and in SBN rats. The expression of the alpha 2B subtype was permanently higher in the SBH rats than in the SBN rats. The expression of the alpha 2A gene in the SBH rats suggests a specific SBH post-transcriptional regulation resulting in the absence of alpha 2A-adrenoceptor. CONCLUSIONS: Differences exist in the renal cortex concerning expression and distribution of alpha 2-adrenoceptor subtypes between SBH and SBN rats. From these differences there might result different alpha 2-adrenoceptor-mediated renal functions in SBH and in SBN rats, which could lead to a predisposition to sensitivity or resistance to a high sodium intake.

Animals↗
PubMed1997

Enhanced electrical activity in mesenteric arteries from salt-loaded Dahl salt-sensitive rats: actions of prostaglandin H2 on membrane channels.

Salt loading increases blood pressure in Dahl salt-sensitive (Dahl S) rats. We have previously shown that the mesenteric artery of salt-loaded Dahl S rats exhibits enhanced electrical activity that is corrected by a cycloxygenase inhibitor, indomethacin. Prostaglandin H2 (PGH2) is a product of cycloxygenase that is known as an intrinsic vasoconstricting factor in spontaneously hypertensive rats. Our hypothesis is that tissue production of PGH2 would be involved in the enhanced electrical activity of arteries from salt-loaded Dahl S rats. In the present study, to clarify this possibility, we evaluated the actions of PGH2 on membrane channels in arterial cells from Dahl S rats. Membrane currents were recorded by whole-cell voltage clamp technique in single smooth muscle cells from the mesenteric artery. Application of PGH2 evoked an inward current that was mainly dependent on extracellular Na+ in the physiological extracellular solution. When high Ba2+ solution was used for the extracellular solution, PGH2 also evoked the inward current, suggesting that a divalent cation, such as Ba2+ or Ca2+, could permeate the PGH2-activated channels. In contrast, the L-type Ca2+ channel currents were not enhanced by the application of PGH2. The present results suggest that production of PGH2 contributes to the enhanced electrical activity by activating cation-permeable channels and depolarizing the membrane potential. PGH2 also directly stimulates the Ca2+ influx by activating Ca2+ permeable channels.

Animals↗
PubMed1999

Some magnesium salts and a mixture of magnesium and calcium salts accelerate skin barrier recovery.

The effects of four different magnesium salts on the cutaneous barrier recovery rate after barrier disruption were evaluated. We spread an aqueous solution of each salt on the flank skin of hairless mice, occluded the area with a plastic membrane for 20 min, and then left the skin surface to dry. All of the magnesium salts, except magnesium bis(dihydrogen phosphate), accelerated barrier repair. We next estimated the effects of magnesium chloride aqueous solutions which contained calcium chloride at different molar ratios. When the calcium to magnesium ratio was lower than 1, the mixture accelerated barrier repair. The application of an aqueous solution of 10 mM magnesium chloride and 10 mM calcium chloride was found to hasten the barrier recovery more effectively than a solution of 10 mM magnesium chloride. These results suggest that the effects of these metal ions are different depending on the counter ion and/or the method of application.

Animals↗