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PubMed2000

The circadian rhythm of blood pressure and the effect of salt intake in salt-sensitive subjects.

OBJECTIVE: To investigate the effect of salt intake on the circadian rhythm of blood pressure and the characteristics of ambulatory blood pressure (ABP) in salt-sensitive (SS) subjects. METHODS: Twenty-three normotensive subjects and forty-three patients with essential hypertension were included in this study. Salt sensitivity was determined with a chronic dietary salt loading test and an acute venous saline loading test, respectively. 24-hour ABP measurements were performed twice in normotensive subjects when they were on a high salt diet and when they had a low salt diet. Blood and urine samples were collected for measurement of plasma norepinephrine concentration (PNE), plasma renin activity (PRA), angiotensin II, aldosterone, erythrocyte sodium content and urinary sodium excretion. 24-hour ABP readings were also obtained in patients with essential hypertension when antihypertensive drugs were discontinued for at least 2 weeks. RESULTS: High salt intake attenuated the circadian rhythm of blood pressure in SS normotensive subjects, and the nocturnal decline in blood pressure was smaller in SS patients with essential hypertension than in salt-resistant (SR) patients. The level of PNE was higher and the suppression of PRA was smaller in SS subjects than in SR subjects when they had a high salt diet, and the urinary sodium excretion decreased and the erythrocyte sodium content increased significantly in SS subjects on high salt intake. CONCLUSIONS: High salt intake caused an abnormal circadian rhythm of blood pressure in SS subjects. The blunted nocturnal decline in blood pressure may be a characteristics of SS patients with essential hypertension.

Adult↗
PubMed1991

Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults.

Evidence suggests that dietary salt reduction similar to diuretic therapy may adversely affect lipid and glucose metabolism. We studied 147 non-obese normotensive subjects (60 females and 87 males) aged 19-78 years who entered a single-blind crossover trial and were randomly assigned to a low salt diet of 20 mmol or a high salt diet of 300 mmol sodium per day, for 7 days each. Sodium restriction lowered mean arterial blood pressure (MAP) by a mean of 7.5 mmHg in 17% (salt-sensitive), had no hemodynamic effect in 67% (salt-resistant) and raised MAP by a mean of 6 mmHg in 16% of the subjects (reverse reactors). With dietary salt restriction serum total- and LDL-cholesterol as well as serum insulin and uric acid concentrations increased significantly in all three groups. The largest increases in total (10%) and LDL- (12%) cholesterol occurred in the reverse reactors. Salt-sensitives had significant higher lipoprotein(a) values than the other two groups. Salt-restriction had no significant effect on this parameter. Plasma renin activity, as well as plasma aldosterone and noradrenaline concentrations rose in all three groups during the low salt diet, the largest increases being observed in the reverse reactors. Short-term sodium restriction in normotensive adults has unfavourable effects on lipid and glucose metabolism, especially in subjects who do not derive hemodynamic benefit. Further studies are necessary to examine the effects of more moderate salt reduction for longer periods on the risk factor profile for cardiovascular disease before a low salt diet can be regarded as a safe public health measure for the general population.

Adult↗
PubMed1987

Salt consumption and the effect of salt on mineral metabolism in horses.

The voluntary salt consumption of mature unexercised horses was measured weekly for up to 45 weeks. Voluntary intake among horses was quite variable ranging from 19 to 143 g of salt per day and was inversely related to total salt intake (salt in feeds plus voluntary intake). Mean daily voluntary salt consumption was 53 g. Season of the year did not influence voluntary intake. In preference tests which evaluated every two choice combination of 0.2% and 4% NaCl in test diets fed daily for four days, ponies generally preferred diets containing the lower amount of salt. In similar preference studies which used NaHCO3 as a sodium source, ponies always preferred the diet containing the lower level of NaHCO3. Metabolism studies employing diets containing 1, 3 or 5% NaCl showed that urinary excretion was the major excretory pathway for sodium and chloride. Fecal excretion, intestinal absorption and retention of sodium were not affected by level of salt intake. Urinary calcium excretion was unaffected by salt intake but calcium and phosphorus absorption and retention were enhanced when ponies were fed diets containing 3 or 5% sodium chloride. Magnesium and copper metabolism were unaffected by salt intake. Horses voluntarily consume relatively large amounts of sodium chloride but it is likely that not all voluntary consumption is related to the salt requirement of the horse. Habit and taste preference could also be involved. Salt consumption at the levels used in these studies does not appear to be detrimental to the metabolism of other minerals in the horse.

Animals↗
PubMed1997

Beneficial effects of long-term enalapril treatment and low-salt intake on survival rate of dahl salt-sensitive rats with established hypertension.

We investigated the effects of long-term treatment with the angiotensin-converting enzyme inhibitor enalapril and low-salt intake on the survival rate of Dahl salt-sensitive rats fed a high-salt (6.0% NaCl) diet. The systolic blood pressure of the rats increased gradually from 5 weeks of age and reached >240 mm Hg at 12 weeks of age. At this point, a low-salt diet group received a placebo (group 1, n = 10), and the high-salt diet group was divided into three groups: those given a placebo with the high-salt diet (group 2, n = 15), those given a chow change from a high- to a low-salt diet with a placebo (group 3, n = 14) and those given enalapril (30 mg/kg/day p.o., group 4, n = 14). At 19 weeks of age, all rats in group 1 were alive, and the survival rate of group 2 was only 40% (P < .001 vs. group 1). The survival rates of both groups 3 and 4 were significantly better: 86% (P < .01 vs. group 2) and 93% (P < .01), respectively. This beneficial effect on mortality was accompanied by an amelioration of the elevated plasma creatinine and urea nitrogen levels and a decrease in the glomerular sclerosis lesion scores in both groups. These results suggested that a high-salt content diet and the renin-angiotensin system are deterioration factors in lethal renal damage and the limitation of the diet salt content and inhibition of the renin-angiotensin system are important to improve the survival rate in high-salt-loaded hypertensive Dahl salt-sensitive rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Activity coefficients of salts in highly concentrated protein solutions. II. Potassium salts in isoionic bovine serum albumin solutions.

Mean activity coefficients of different potassium salts KX (X = F-, Cl-, Br-, I-, NO3-, SCN-) have been measured in concentrated isoionic bovine serum albumin (BSA) solutions, by use of the EMF method with ion-exchange membrane electrodes. These solutions may be regarded as simple model systems for the cytoplasm of living cells as far as the influence of the macromolecular component on the activity coefficients of the salts is concerned. Two series of measurements have been carried out: (a) varying the amount of salt from 0.01 to 0.5 molal and maintaining the BSA concentration constant at 20 wt% and (b) varying the protein concentration up to 25 wt% and keeping the salt concentration constant at 0.1 molal. For all salts studied, the mean activity coefficients in the protein-salt solutions increase as the salt concentration rises, when the protein concentration is maintained constant. In the series of measurements (b) the activity coefficients of all salts change linearly with the protein concentration. Marked qualitative differences, however, were observed depending on the anion species, which could be interpreted in terms of specific ion binding of X- to the protein molecule. By taking into account BSA-bound 'non-solvent' water, the results were analyzed in terms of numbers of anions bound per BSA molecule. Comparison with the results of Scatchard, obtained at low protein concentrations, showed only a very small electrostatic effect of the BSA-(X-)v polyions on the activity coefficient of the salts at higher protein and salt concentrations.

Kinetics↗
PubMed1999

Partial characterization of mechanisms of cytoprotective action of hydrophilic bile salts against hydrophobic bile salts in rats: relation to canalicular membrane fluidity and packing density.

Bile salts regulate the subselection of phosphatidylcholine species secreted into bile and thereby modulate bile metastability. The aim of this study was to determine whether bile salts alter phosphatidylcholine species of the canalicular membrane, and if they do, to clarify whether the cytoprotective action of hydrophilic bile salts is associated with modulation of phosphatidylcholine composition in cell membrane bilayers. Bile salt-pool-depleted rats were infused intravenously with sodium taurocholate at a constant rate (200 nmol/min/100 g body wt) for 2 hr, followed by infusion of either sodium tauroursodeoxycholate, sodium tauroalphamuricholate, or sodium taurobetamuricholate (200 nmol/min/100 g) for 2 hr. Biliary outputs of cholesterol and phosphatidylcholine and phosphatidylcholine hydrophobicity in bile and subcellular fractions were determined. The cytoprotective action of hydrophilic bile salts was determined by the release of canalicular membrane-localizing enzymes (alkaline phosphatase, leucine aminopeptidase) into bile. Tauroursodeoxycholate, taurobetamuricholate, and tauroalphamuricholate decreased the release of these enzymes when compared to values under taurocholate infusion. Bile phosphatidylcholine hydrophobicity was also decreased by the bile salts, whereas the cholesterol/phosphatidylcholine ratio was increased. In contrast, phosphatidylcholine hydrophobicity in the canalicular membrane was increased by these three bile salts. In conclusion, hydrophilic bile salts promote biliary secretion of relatively hydrophilic phosphatidylcholine secretion into bile, and consequently phosphatidylcholine hydrophobicity in canalicular membranes increased. Such an alteration in phosphatidylcholine species within canalicular membrane enhances its lateral packing density with less fluidity, and this may account, in part, for the cytoprotective action of hydrophilic bile salts against hydrophobic bile salts.

Animals↗
PubMed1977

Bile salt metabolism. II. Bile salts and disease.

Alterations of bile salt metabolism have been shown in numerous diseases. Liver damage results in elevated serum bile salt concentrations which may be useful as a sensitive index of hepatocellular disease. Changes in the relative proportions of the individual bile salts in serum occur with cholestasis. Urinary excretion of bile salts, largely in the form of sulphates, increases as a compensatory mechanism. Ileal disease or resection causes bile salt melabsorption. The increase in colonic bile salts produces a watery diarrhoea while the decrease in duodenal levels may cause steatorrhoea. Cholelithiasis may result from alteration in the relative proportions of cholesterol, lecithin and bile salts in bile. The mechanism apparently differs in various conditions predisposing to gallstone formation. A primary alteration of bile salt metabolism has been postulated in several other conditions. Considerable interest centres on the importance of metabolites of bile salts in the pathogenesis of colonic carcinoma. Chenodeoxycholic acid is a successful though costly treatment for selected patients with cholesterol gallstones. Bile salt binding agents, such as cholestyramine, are extremely useful especially in the control of pruritus in patients with cholestasis.

Animals↗
PubMed1982

Regulation of bile salt transport in rat liver. Evidence that increased maximum bile salt secretory capacity is due to increased cholic acid receptors.

Expansion of the bile salt pool size in rats increases maximum excretory capacity for taurocholate. We examined whether increased bile salt transport is due to recruitment of centrolobular transport units or rather to adaptive changes in the hepatocyte. Daily sodium cholate (100 mg/100 g body wt) was administered orally to rats. This treatment was well tolerated for at least 4 d and produced an 8.2-fold expansion of the bile salt pool. This expanded pool consisted predominently (99%) of cholic and deoxycholic acids. Significantly increased bile salt transport was not observed until 16 h after bile acid loading, and maximum elevations of transport capacity to 2.3-fold of control required approximately 2 d. In contrast, maximum sulfobromophthalein excretion rates increased 2.2-fold as early as 4 h and actually fell to 1.5-fold increase at 4 d. We studied the possibility that this adaptive increase in bile salt secretory transport was due to changes in canalicular surface membrane area, lipid composition, or increased number of putative carriers. Canalicular membrane protein recovery and the specific activities of leucine aminopeptidase, Mg(++)-ATPase and 5'-nucleotidase activities were unaltered by bile salt pool expansion. The content of free and esterified cholesterol and total phospholipids was unchanged in liver surface membrane fractions compared with control values. In contrast, sodium cholate administration selectively increased specific [(14)C]cholic acid binding sites twofold in liver surface membrane fractions. Increased numbers of [(14)C]cholic acid receptors (a) was associated with the time-dependent increase in bile salt transport, and (b) was selective for the taurine conjugate of cholate and (c) was reduced by chenodeoxycholate. Changes in bile acid binding sites 16 h following taurocholate and chenodeoxycholate and the lack of change with glycocholate was associated with comparable changes in bile salt transport. In conclusion, selective bile salts increase bile salt transport in the liver through an adaptive increase in the density of putative bile acid carriers in liver surface membrane.

Animals↗
PubMed1987

Binding characteristics of atrial natriuretic factor and the production of cyclic GMP in kidneys of Dahl salt-sensitive and salt-resistant rats.

The binding of atrial natriuretic factor (ANF) was studied in kidney membranes of inbred salt-sensitive (S) and inbred salt-resistant (R) rats on high or low salt diet. Important differences between strains were seen in the rate of dissociation of ANF from its renal receptor(s) and this was dependent on salt (NaCl) intake. On low salt diet ANF dissociation rates were similar between strains. R rats responded to high salt diet with a decrease in the rate of ANF dissociation from its renal receptor, but ANF dissociation in S rats was not altered by dietary salt. Receptor density was similar between strains. Basal cGMP production was slightly higher for renal membranes of S rats, but ANF stimulation of cGMP production was similar between strains and was not influenced by salt intake in either strain. Since strain-related salt-induced changes in ANF-receptor binding kinetics were not reflected in any strain-related salt-induced changes in ANF stimulated cGMP production, it is tentatively concluded that the ANF receptor likely to be different between S and R strains is the ANF receptor not linked to cGMP production.

Animals↗
PubMed2003

Origin and spoilage potential of the microbiota dominating genus Psychrobacter in sterile rehydrated salt-cured and dried salt-cured cod (Gadus morhua).

Salt-cured and dried salt-cured cod rehydrated using sterile water and equipment have a short shelf life at 4 degrees C due to high bacterial counts. The microbiota develops off-odours which partly can be described as musty, causing sensory rejection within 7-10 days of chilled storage. The microbiota composition was studied in a total of 38 samples obtained from 10 different, both commercial and laboratory produced, salt-cured and dried salt-cured cod products. The dominating bacterium, representing at least 90% of the total viable count in all products studied, was identified as belonging to the genus Psychrobacter; a Gram-negative, oxidase- and catalase-positive, nonpigmented, halotolerant, psychrotolerant, facultative aerobe and nonmotile bacterium. The morphology of the bacterium resembles coccobacilli and the cells occur most often in pairs. The bacterium was able to hydrolyze lipids, but not proteins. It did not produce H(2)S or TMA and the spoilage in rehydrated salt-cured and dried salt-cured cod is therefor different from what is observed in fresh cod. However, samples inoculated with Psychrobacter immobilis gave the same musty odour as spoiled control samples but earlier in the storage period and of a stronger intensity. In a field experiment, carried out to investigate the origin of the dominating bacterium, it was found that the microbiota in both sterile rehydrated commercially produced and laboratory (aseptically) produced salt-cured cod was dominated by this same bacterium. The bacterium was also isolated from cod skin mucus immediately after capture. The bacterium survived NaCl concentrations up to 25% (w/v) NaCl, stating its ability to survive during the salt-curing process. The dominating bacterium in rehydrated salt-cured and dried salt-cured cod seems to mainly originate from the fresh fish itself and not from contamination during processing.

Animals↗
PubMed2002

Salt stress induces up-regulation of an efficient chloroplast antioxidant system in the salt-tolerant wild tomato species Lycopersicon pennellii but not in the cultivated species.

The response of the chloroplastic antioxidant system of the cultivated tomato Lycopersicon esculentum (Lem) and its wild salt-tolerant related species L. pennellii (Lpa) to NaCl stress was studied. An increase in H2O2 level and membrane lipid peroxidation was observed in chloroplasts of salt-stressed Lem. In contrast, a decrease in these indicators of oxidative stress characterized chloroplasts of salt-stressed Lpa plants. This differential response of Lem and Lpa to salinity, correlates with the activities of the antioxidative enzymes in their chloroplasts. Increased activities of total superoxide dismutase (SOD), ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), glutathione-S-transferase (GST), phospholipid hydroperoxide glutathione peroxidase (PHGPX) and several isoforms of non-specific peroxidases (POD) were found in chloroplasts of salt-treated Lpa plants. In these chloroplasts, in contrast, activity of lipoxygenase (LOX) decreased while in those of salt-stressed Lem it increased. Although total SOD activity slightly increased in chloroplasts of salt-treated Lem plants, differentiation between SOD types revealed that only stromal Cu/ZnSOD activity increased. In contrast, in chloroplasts of salt-treated Lpa plants FeSOD activity increased while Cu/ZnSOD activity remained unchanged. These data indicate that salt-dependent oxidative stress and damage, suffered by Lem chloroplasts, was effectively alleviated in Lpa chloroplasts by the selective up-regulation of a set of antioxidative enzymes. Further support for the above idea was supplied by leaf discs experiments in which pre-exposure of Lpa plants to salt-treatment conferred cross-tolerance to paraquat-induced oxidative stress while increased oxidative damage by paraquat-treatment was found in salt-stressed Lem plants.

Journal Article↗
PubMed2004

Salt and salted food intake and subsequent risk of gastric cancer among middle-aged Japanese men and women.

Evidence on the association between salt intake and gastric cancer is sparse, especially in prospective studies. We conducted a population-based prospective study in Japan, where the majority of men has been infected with Helicobacter pylori. A total of 18 684 men and 20 381 women aged 40-59 years who reported their dietary habits and did not report any serious disease at baseline were followed from 1990 to 2001. A total of 486 cases, 358 men and 128 women, with histologically confirmed gastric cancer were documented among them. The quintile category of salt intake was dose-dependently associated with gastric cancer risk in men after adjusting for potential confounding factors (P for trend <0.001), while a trend was not clear in women (P for trend=0.48). Although stratification by study area, with varied salt intake and gastric cancer incidence, attenuated the observed clear associations with salt and salted foods, the frequency categories of highly salted foods such as salted fish roe and salted fish preserves were strongly associated with the risk in both sexes. Restriction of salt and salted food intake is a practical strategy to prevent gastric cancer in areas with high risk.

Age Factors↗
PubMed1997

Role of eicosanoids in alteration of membrane electrical properties in isolated mesenteric arteries of salt-loaded, Dahl salt-sensitive rats.

1. The role of eicosanoids in altered membrane electrical properties of Dahl salt-sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt-resistant (DR) rats fed either a high or low salt diet. 2. The membrane was significantly depolarized in salt-loaded DS rats compared with the other three groups. In addition, the arteries of salt-loaded DS rats exhibited spontaneous electrical activity. 3. Spontaneous electrical activity in salt-loaded DS rats was inhibited by the following: indomethacin, a cyclo-oxygenase inhibitor; ONO-3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY-046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca(2+)-channel antagonist and by Ca(2+)-free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin. 4. Membrane potential in arteries of salt-loaded DS rats was not affected by either indomethacin or ONO-3708. 5. Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt-loaded DS rats. 6. These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage-dependent Ca(2+)-channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt-loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt-loaded DS rats. Mechanisms of depolarization remain to be determined.

Animals↗
PubMed2005

Salt, salted food intake, and risk of gastric cancer: epidemiologic evidence.

Because gastric cancer is still the most common cancer, its prevention is one of the most important aspects of Japan's cancer control strategy. Observations among Japanese immigrants in the USA and Brazil based on the geographic differences, the trend in cancer incidence with time, and the change in incidence patterns indicate that gastric cancer is closely associated with dietary factors, such as the intake of salt and salted food. In international and intra-Japanese ecological studies, the average salt excretion level, estimated using randomly selected 24-h urine samples in each population, was closely correlated with gastric cancer mortality. Several case-control and cohort studies, including the author's recent works, have shown that a higher intake of some traditional salt-preserved food and salt per se, which was estimated using a validated food-frequency questionnaire, was associated with a risk of gastric cancer. While salted food intake may increase the risk of Helicobacter pylori infection, it can also act synergistically to promote the development of gastric cancer. Based on substantial evidence about the association between salt and salted food intake and the risk of gastric cancer from ecological, case-control, and cohort studies conducted in Japan and other countries, as well as mechanistic plausibility, dietary modification involving less salt and salted food intake is a practical strategy with which to prevent gastric cancer.

Adult↗
PubMed1987

Prenatal high salt diet increases blood pressure and salt retention in the spontaneously hypertensive rat.

1. An examination was made of the effect of prenatal, high salt (5% w/w) and low salt (0.1% w/w) diet on the blood pressure and ability to excrete a salt load of mature spontaneously hypertensive rats (SHR) of the Okamoto strain maintained on normal salt (0.8% w/w) diet after weaning. 2. Prenatal high salt diet resulted in a significant exacerbation of the hypertension of 4 month old SHR when compared with animals given prenatal low salt diet. 3. Three month old SHR given prenatal, high salt diet exhibited a significantly reduced Na+ excretion following a single, oral salt load (150 mmol/l, 1% bodyweight) when compared with the low salt group. 4. Thus, prenatal, high salt diet may influence body fluid homeostasis in genetically susceptible individuals later in life.

Animals↗
PubMed1992

Sodium and noradrenaline in cerebrospinal fluid and blood in salt-sensitive and non-salt-sensitive essential hypertension.

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.

Adult↗
PubMedDate not supplied

Sodium balance and jejunal ion and water absorption in Dahl salt-sensitive and salt-resistant rats.

1. Apparent Na+ absorption and jejunal water, Na+, Cl- and K+ absorption in vivo was evaluated in young (prepubertal) and adult Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats kept on a low-salt (low-salt rat chow + distilled water) or a high-salt diet (HS1 diet: NaCl-enriched rat chow + distilled water; HS2 diet: standard rat chow + 1% saline as drinking fluid). These two high-salt diets were chosen because the HS1 regimen has been shown to increase blood pressure (BP) in DS rats and the HS2 regimen decreases jejunal water and ion absorption in normotensive Wistar rats. 2. The HS1 or HS2 diet increased BP in young and adult DS rats but had no effect on the BP of young and adult DR rats. 3. Irrespective of dietary Na+ intake, no significant difference of apparent Na+ absorption (dietary Na+ intake minus faecal Na+ output) was observed between DS and DR rats both in prepuberty and in adulthood. Young DS rats kept on a low-salt diet had increased faecal Na+ output in comparison with young DR rats. This difference disappeared with increasing dietary Na+ intake. 4. There were no interstrain differences on the effect of a high-salt diet on jejunal Na+ and K+ absorption in young and adult DS and DR rats. However, high-salt diets stimulated jejunal water and Cl- absorption in young DS rats, but not in adult DS rats and young and adult DR rats. Interstrain differences of water and Cl- absorption were observed only in adulthood. Adult DR rats kept on an HS2 diet absorbed more water and Cl- than their DS counterparts. 5. Our results do not indicate any abnormalities of apparent Na+ absorption and jejunal water and electrolyte transport in DS and DR rats. We conclude that there is no relationship between intestinal Na+ absorption and sensitivity or resistance to induction of experimental salt hypertension.

Age Factors↗
PubMed2004

Heme oxygenase-derived carbon monoxide promotes arteriolar endothelial dysfunction and contributes to salt-induced hypertension in Dahl salt-sensitive rats.

Vascular tissues express heme oxygenase (HO), which metabolizes heme to form carbon monoxide (CO). Heme-derived CO inhibits nitric oxide synthase and promotes endothelium-dependent vasoconstriction. After 4 wk of high-salt diet, Dahl salt-sensitive (Dahl-S) rats display hypertension, increased vascular HO-1 expression, and attenuated vasodilator responses to ACh that can be completely restored by acute treatment with an inhibitor of HO. In this study, we examined the temporal development of HO-mediated endothelial dysfunction in isolated pressurized first-order gracilis muscle arterioles, identified the HO product responsible, and studied the blood pressure effects of HO inhibition in Dahl-S rats on a high-salt diet. Male Dahl-S rats (5-6 wk) were placed on high-salt (8% NaCl) or low-salt (0.3% NaCl) diets for 0-4 wk. Blood pressure increased gradually, and responses to an endothelium-dependent vasodilator, ACh, decreased gradually with the length of high-salt diet. Flow-induced dilation was abolished in hypertensive Dahl-S rats. Acute in vitro pretreatment with an inhibitor of HO, chromium mesoporphyrin (CrMP), restored endothelium-dependent vasodilation and abolished the differences between groups. The HO product CO prevented the restoration of endothelium-dependent dilation by CrMP. Furthermore, administration of an HO inhibitor lowered blood pressure in Dahl-S rats with salt-induced hypertension but did not do so in low-salt control rats. These results suggest that hypertension and HO-mediated endothelial dysfunction develop gradually and simultaneously in Dahl-S rats on high-salt diets. They also suggest that HO-derived CO underlies the impaired endothelial dysfunction and contributes to hypertension in Dahl-S rats on high-salt diets.

Acetylcholine↗