Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NaCl”

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
PubMed1992

Effects of acute and chronic blockade of neutral endopeptidase with Sch 34826 on NaCl-sensitive hypertension in spontaneously hypertensive rats.

We have previously demonstrated that dietary NaCl supplementation is associated with increased circulating atrial natriuretic peptide (ANP) levels in Wistar-Kyoto (WKY) rats but not in spontaneously hypertensive rats (SHR), and that replacement with exogenous ANP prevents NaCl-sensitive hypertension in NaCl-sensitive SHR (SHR-S). The current study tested the hypothesis that chronic administration of the neutral endopeptidase (NEP) inhibitor Sch 34826 prevents NaCl sensitive hypertension in SHR-S by increasing endogenous ANP. Male SHR-S received Sch 34826 (90 mg/kg/day) or vehicle by gavage for 4 weeks beginning immediately before the initiation of 1% or 8% NaCl diets at age 7 weeks. Sch 34826 prevented the increase in arterial pressure in response to 8% NaCl in SHR-S, but had no effect on blood pressure in 1% NaCl fed SHR-S; plasma ANP levels were increased by 63 and 68% in the 1% and 8% NaCl groups, respectively, in response to Sch 34826. To examine the mechanism(s) of the antihypertensive effect of Sch 34826 in NaCl-supplemented SHR-S, a single dose (90 mg/kg) of Sch 34826 or vehicle was administered by gavage to SHR-S that had consumed 1% or 8% NaCl diets for 3 weeks. Sch 34826 abolished the NaCl-induced increase in blood pressure 3 h after treatment in 8% NaCl fed SHR-S, but had no effect in SHR-S fed the 1% NaCl diet. This effect was associated with increased urine volume and urinary sodium, ANP, and cyclic GMP in 8% NaCl fed SHR-S.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Antihypertensive effect of cicletanine is exaggerated in NaCl-sensitive hypertension.

Cicletanine (CIC), a furopyridine derivative, lowers blood pressure in hypertensive animals and humans. We have previously identified an NaCl-sensitive substrain of spontaneously hypertensive rat (SHR-S) that displays enhanced sensitivity to the depressor effects of exogenous atrial natriuretic peptide (ANP) when fed a high NaCl diet. The current study tested the hypotheses that CIC has an exaggerated antihypertensive effect in NaCl-supplemented SHR-S and that this effect might be ANP dependent. CIC (40 mg/kg/day) or vehicle was administered by gavage in a single daily dose for three weeks beginning immediately prior to initiation of 1% or 8% NaCl diets in seven-week-old male SHR-S. CIC significantly decreased mean arterial pressure (MAP) and the ratio of left ventricular and septum weight to body weight (LV + S/BW) in both 8% NaCl- and 1% NaCl-fed SHR-S. The depressor effect of CIC was greater in the 8% NaCl group (-26 mmHg) than in the 1% NaCl group (-13 mmHg). CIC was associated with significant reduction in RAP in the 8% NaCl group but not in the 1% NaCl group. Neither CIC treatment nor 8% NaCl significantly altered plasma ANP or cyclic guanosine monophosphate (GMP) levels in plasma, aorta, or kidney. CIC was associated with significant decreases in plasma norepinephrine (NE) levels in the 1% NaCl group but not in the 8% NaCl group. The data demonstrate that the antihypertensive effect of CIC is exaggerated in NaCl-sensitive hypertension. The antihypertensive effect of CIC appears not to be related to ANP or cyclic GMP but may be related to a combination of a sympatholytic and natriuretic/diuretic effects in SHR-S.

Animals↗
PubMed1988

Osmolality, NaCl dietary intake, and regulation of ventilation by CO2.

The ventilatory response to CO2 (VR) was examined in six awake dogs during the 2nd week of sequential dietary periods of low NaCl (less than 5 meq NaCl/day), high NaCl (approximately 120 meq NaCl/day), and then repeated low NaCl. Water intake was maintained constant at 77 ml.kg-1.day-1. PCO2 of arterial blood (PaCO2) and the PaCO2 threshold of the VR increased between the high-NaCl and the second low-NaCl period; the PaCO2 threshold did not change between the first low-NaCl and the high-NaCl period. In contrast, arterial [H+] ([H+]a) threshold of the VR increased between the first low-NaCl period and the high-NaCl period, but did not change further in the second low-NaCl period. Variations in [H+]a threshold of the VR between dogs on high- and low-NaCl diets were correlated with plasma osmolality, and this accounted for a positive linear relation between [H+]a and plasma osmolality. During the high-NaCl period, the arterial strong ion difference [[SID]a = ([Na+] + [K+]) - ([lactate-] + [Cl-])] decreased, forcing [H+]a to increase. However, during high-NaCl diet, PaCO2 decreased relative to plasma osmolality, counterbalancing the decrease in [SID]a and maintaining the relation between [H+]a and plasma osmolality. The compensatory mechanism for the decrease in PaCO2 during high NaCl was a shift in the relation between PaCO2 threshold of the VR and plasma osmolality to a lower PaCO2 threshold. Chemoreceptor, osmoreceptor, and/or humoral mechanisms are potentially involved in these respiratory adaptations to alterations in electrolyte and water balance.

Animals↗
PubMed1984

Effects of butylated hydroxyanisole, butylated hydroxytoluene, and NaCl on gastric carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine in F344 rats.

Promoting activities of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), and NaCl and of combinations of these antioxidants with NaCl on gastric carcinogenesis initiated by N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) (CAS: 70-25-7; 1-methyl-3-nitro-1-nitrosoguanidine] were investigated in male inbred F344 rats. Animals, 6-week old, were given an intragastric administration of MNNG at 150 mg/kg body weight by gastric tube and 1 week later were placed on a diet containing BHA (0.5%), BHT (1.0%), NaCl (5.0%), BHA (0.5%) plus NaCl (5%), or BHT (1.0%) plus NaCl (5.0%) for 51 weeks. Control rats received no further treatment after MNNG administration. A single intragastric application of MNNG to rats induced multiple epithelial tumors of the forestomach and a few epithelial tumors of the glandular stomach after 52 weeks. Squamous cell carcinomas of the forestomach were seen in 2 of 18 effective rats (11.1%) in the control groups, and the incidences in the groups receiving the subsequent treatment were 45.0% with BHA, 15.8% with BHT, 30% with NaCl, 70% with BHA plus NaCl, and 52.9% with BHT plus NaCl. Differences in the incidences of squamous cell carcinoma between the controls and groups given BHA, BHA plus NaCl, and BHT plus NaCl were statistically significant. NaCl given alone after MNNG administration also significantly increased the incidence of papillomas in the forestomach. Incidences of glandular stomach tumors, adenomas and carcinomas were not affected by any of the subsequent treatments. No tumors of the stomach developed in the groups given BHA, BHT, and NaCl without MNNG pretreatment. Thus the present experiment revealed that BHA and NaCl but not BHT exert promoting activity on MNNG-induced forestomach carcinogenesis in rats and that, when BHA and BHT were given with NaCl, promotion was more marked, suggesting a synergistic effect on tumor promotion.

Animals↗
PubMed2002

NaCl-induced oxidative damage in the cyanobacterium Anabaena doliolum.

Results obtained with graded concentrations of NaCl (20-200 m M) show decrease in the chlorophyll 'a' contents of Anabaena with increasing concentration of NaCl except at extremely low concentration of NaCl (5-20 m M). The rate of Hill activity and oxygen evolution are found to be stimulated by lower concentrations of NaCl, but not at higher concentrations of NaCl. Results have demonstrated that the O(2) evolution process is relatively more sensitive to NaCl stress than the Hill activity. Further, the results show NaCl induced an increase in the rate of RNO bleaching and loss of total thiol (-SH) contents. Taken together, these results suggest a NaCl-induced general oxidative stress. Results on the effect of oxygen radical quenchers reveal a predominant role of singlet oxygen in the NaCl-induced general oxidative stress as evident from a higher quenching effect of sodium azide than formate and histidine on the rate of RNO bleaching in Anabaena cells. However, the rate of lipid peroxidation and SOD activity show a declining pattern in response to increasing concentrations of NaCl. There is the possibility of a NaCl-induced decrease in the rate of lipid peroxidation when the SOD activity is also lower. But the NaCl-induced decline in the SOD activity does suggest that symptoms of general oxidative stress at elevated levels of NaCl are apparently owing to collapse of intracellular defense of the cells against the toxic oxygen radicals, not because of the higher rate of photosynthetic activity.

Anabaena↗
PubMed2001

NaCl preference increases during pregnancy and lactation: assessment using brief access tests.

Pregnancy and lactation are characterized by increases in NaCl intake, as determined by long-term consumption tests, which cannot examine the relative contribution of taste and postingestive factors to this phenomenon. Consequently, in this study, changes in NaCl preference during pregnancy and lactation were studied in nulliparous Long-Evans rats using a brief access test (lickometer). In Experiment 1, rats were maintained on a Na(+)-adequate diet (0.03% Na(+)), habituated to lickometer testing, and subsequently assessed during pregnancy and lactation with three 30-s exposures to each of seven taste solutions: 0.075 M sucrose (base), 0.089 M NaCl in base, 0.158 M NaCl in base, 0.281 M NaCl in base, 0.5 M NaCl in base, 0.158 M NaCl and 0.281 M NaCl. Results indicated higher lick rates to the 0.5 M NaCl in base, 0.158 M NaCl and 0.281 M NaCl solutions during late pregnancy and late lactation (Day 13 and beyond). In Experiment 2, a comparison of two diets differing in sodium content (0.03% vs. 0.3% Na(+)) determined that these changes in NaCl preference during pregnancy and lactation were unrelated to dietary sodium. Thus, the apparent increase in NaCl preference during pregnancy and lactation, independent of dietary sodium, suggests that this change in preference is not in response to physiological sodium need.

Animals↗
PubMed1987

Dietary NaCl determines severity of potassium depletion-induced metabolic alkalosis.

It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce and sustain a small decrease in blood acidity and increase in plasma bicarbonate concentration; we hypothesized that more severe alkalosis was prevented by mitigating mechanisms initiated by renal retention of dietary NaCl that was induced by K+ depletion. To ascertain the acid-base response to dietary K+ depletion under conditions in which the availability of NaCl for retention is greatly limited, in the present study of six normal men we restricted dietary K+ as in the previous study except that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl Group) instead of high (126 mEq/day, High NaCl Group). Plasma acid-base composition and renal net-acid excretion (NAE) did not differ significantly between groups during the control period. In the steady state of K+ depletion (days 11 to 15 of K+ restriction), neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/- 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/- 48 mEq) differed significantly between groups. During K+ restriction, persisting metabolic alkalosis developed in both groups, which was more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0 mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less than 0.003. A significantly more severe alkalosis in the Low NaCl Group was evident at all degrees of K+ deficiency achieved during the course of the 15 days of K+ restriction, and the severity of alkalosis in the Low NaCl Group correlated with the degree of K+ deficiency. During the generation of alkalosis (days 1 to 7 of K+ restriction), NAE increased in the Low NaCl Group whereas it decreased in the High NaCl Group. During the maintenance of alkalosis (days 11 to 15), NAE stabilized in both groups after it returned to values approximating the control values. In both groups, urine Cl- excretion decreased during K+ restriction even though Cl- intake had not been changed, with the result that body Cl- content increased negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Dietary Ca2+ increases natriuretic and diuretic responses to volume loading in NaCl-sensitive spontaneously hypertensive rats.

The present study tests the hypothesis that dietary Ca2+ supplementation increases acute diuretic and natriuretic responses to volume loading in the NaCl-sensitive spontaneously hypertensive rat (SHR-S). Seven week old male SHR-S and normotensive Wistar-Kyoto rats (WKY) were fed one of the following diets for 2.5 weeks: basal (0.75% NaCl, 0.68% Ca2+); high NaCl (8% NaCl, 0.68% Ca2+); high Ca2+ (0.75% NaCl, 2.0% Ca2+); and high NaCl and Ca2+ (8% NaCl, 2.0% Ca2+). SHR-S on high Ca2+ and on high NaCl and Ca2+ diets for 2 weeks displayed significantly lower systolic arterial pressures (SAP) than SHR-S on basal and high NaCl diets, respectively. WKY displayed no diet-related change in SAP at any time during the study. After 2.5 weeks on the diets, pre-instrumented, conscious SHR-S and WKY received an intravenous infusion (5% body weight) of isotonic NaCl, and urine was collected through a bladder catheter for a period of 90 min. The infusion did not alter the heart rate or the mean arterial pressure in any group. WKY on the high NaCl diet excreted a significantly greater percentage of the volume and Na+ load than WKY on the basal diet. In contrast, SHR-S on the high NaCl (compared to basal) diet did not display significantly enhanced natriuresis or diuresis. SHR-S on the basal diet displayed excretion rates similar to WKY on the basal diet. Dietary Ca2+ supplementation significantly increased the natriuretic and diuretic responses to saline infusion in SHR-S on the high NaCl diet, but not in SHR-S on the basal diet or in WKY on either diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

High NaCl intake decreases both flow-induced dilation and pressure-induced myogenic tone in resistance arteries from normotensive rats: involvement of cyclooxygenase-2.

The effect of high NaCl diet on resistance arteries is not yet fully documented. In order to assess the effect of NaCl on myogenic tone and flow-induced dilation independent of arterial blood pressure change, we used normotensive rats which did not develop hypertension upon high NaCl intake. Normotensive Wistar Kyoto Rats received a high (8%) or a normal NaCl diet (0.4%). Mesenteric resistance arteries (150 microm, internal diameter) were cannulated in an arteriograph to allow perfusion of arteries under controlled pressure and flow. Pressure-induced myogenic tone was lower in the high NaCl group than in the control group. Cyclooxygenase inhibition with indomethacin and (N-(2-cyclohexyloxy)-4-nitro-phenyl)-methanesulphonamide, 1 micromol/l) NS 398 (specific cyclooxygenase-2 inhibitor) similarly decreased myogenic tone in rats fed high NaCl but had no effect in those fed a normal NaCl diet. Flow-induced dilation was decreased in the high NaCl group. Inhibition of nitric oxide synthesis with N(G)-nitro-L-arginine methyl ester decreased flow-induced dilation in both groups. Indomethacin and NS 398 did not change flow-induced dilation. As shown by immunofluorescence COX-2 was present in the endothelium of arteries from rats with a high NaCl diet but not in those fed a normal NaCl diet. Thus, chronic high NaCl intake decreased both flow-induced dilation and myogenic tone in resistance arteries. The chronic high NaCl did not affect the participation of nitric oxide on flow-induced dilation, but induced the expression of cyclooxygenase-2, which participates in myogenic tone. These results suggest that high NaCl changes flow and pressure mechanosensing processes and strengthen the hypothesis that sodium ions have an important role in both pressure and flow-mechanotransduction in vascular cells.

Animals↗
PubMed1993

High NaCl intake of rat dams alters maternal behavior and elevates blood pressure of adult offspring.

The present study investigated whether differences in maternal NaCl intake altered 1) maternal-pup behavior and 2) the development of dietary obesity and blood pressure level of adult Sprague-Dawley rats maintained on a palatable high-fat/milk (HF/M) diet. Thirteen dams fed high (3%) NaCl and 12 dams fed basal (0.12%) NaCl were observed on postnatal days 2-21 for differences in the number of times spent 1) nursing, 2) in contact with or licking, sniffing, and carrying pups, and 3) in nest building. The offspring were continued on their respective NaCl diets to 30 days postpartum, and then both NaCl groups were fed an intermediate (1%) NaCl diet thereafter. Beginning at 60 days of age, the offspring from each maternal NaCl condition were fed either Agway R-M-H 1000 pelleted food or a HF/M diet for 14 wk. Dams fed 3% NaCl spent significantly more time licking their pups than did dams fed 0.12% NaCl. The adult offspring of dams fed 3% NaCl had a significantly higher level of systolic blood pressure and consumed more calories of sweetened condensed milk on the HF/M diet than did rats raised on 0.12% NaCl. Dietary-induced obesity did not magnify the increase in systolic blood pressure from high maternal NaCl intake. The present results raise the possibility that increased maternal licking may contribute to the increased blood pressure and solution intake that follows from high maternal NaCl intake.

Animals↗
PubMed1990

Atrial natriuretic factor prevents NaCl-sensitive hypertension in spontaneously hypertensive rats.

Our previous studies demonstrated that acute infusion of atrial natriuretic factor (ANF) produces an enhanced depressor response in NaCl-sensitive spontaneously hypertensive rats (SHR-S) fed a high (8%) NaCl diet compared with control SHR-S fed a normal (1%) NaCl diet and that dietary NaCl loading increases circulating ANF levels in Wistar-Kyoto (WKY) rats but not in SHR-S. The current study tested the hypotheses that 1) long-term infusion of ANF at a dose that elevates plasma ANF to levels comparable with those seen in high NaCl-fed WKY rats prevents the NaCl-induced exacerbation of hypertension in SHR-S and 2) ANF lowers blood pressure in this model by a sympatholytic effect. Male SHR-S received infusions of ANF (0.1 microgram/hr) or vehicle intravenously via osmotic minipump for 3 weeks beginning immediately before initiation of 1% or 8% NaCl diets at age 7 weeks. Chronic ANF infusion prevented the increase in arterial pressure in response to a high NaCl diet in SHR-S but had no effect in 1% NaCl-fed SHR-S. Thus, the NaCl-sensitive component of hypertension in SHR-S was more sensitive to ANF than the non-NaCl-sensitive component. Plasma norepinephrine was significantly increased in ANF-treated, 8% NaCl-fed SHR-S compared with vehicle controls, suggesting that ANF did not prevent NaCl-sensitive hypertension by a sympatholytic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Genetic basis of NaCl-sensitive hypertension.

Sensitivity to the pressor effects of dietary NaCl and the depressor effects of dietary Ca2+ is inherited. High NaCl diets accelerate the development and/or exacerbate the severity of hypertension in NaCl-sensitive substrains of spontaneously hypertensive rat (SHR-S) but not in NaCl-resistant substrains of SHR (SHR-R) or in normotensive Wistar-Kyoto (WKY) control rats. High NaCl intake leads to increased circulating noradenaline levels and increased depressor responses to ganglionic blockade in SHR-S but not in SHR-R or WKY rats, indicating that peripheral sympathetic nervous system activity and neurogenic peripheral vascular tone are increased by NaCl supplementation in SHR-S, but not in SHR-R or WKY rats. Further, dietary NaCl loading in SHR-S decreases endogenous noradrenaline stores and noradrenaline release in the anterior hypothalamus, a brain region that contains neurons that give rise to depressor responses when stimulated chemically or electrically. These findings are consistent with the hypothesis that decreased activity of noradrenergic depressor neurons in the anterior hypothalamus may mediate and increase in blood pressure that occurs in NaCl-sensitive animals during dietary NaCl supplementation by releasing tonic inhibition of sympathetic outflow. The exacerbation of hypertension and changes in central noradrenergic activity are observed only in NaCl-loaded SHR-S, not in SHR-R or WKY rats, indicating that these NaCl-induced alterations in central noradrenergic activity are genetically mediated. Dietary Ca2+ supplementation prevents (or reverses) the NaCl-induced changes in blood pressure, peripheral sympathetic nervous system activity, and anterior hypothalamic noradrenaline release in SHR-S, suggesting that dietary NaCl and Ca2+ may have opposing effects on the same regulatory pathway(s). The genetic defect in NaCl/Ca2+ sensitivity of blood pressure is not yet identified, but probably involves cation transport at the cellular level.

Animals↗
PubMedDate not supplied

High dietary NaCl early in development enhances mean arterial pressure of adult rats.

We investigated the long-term influence of early dietary NaCl on adult mean arterial pressure (MAP) and heart rate (HR), assessed continuously for 7 weeks when fed water and chow containing 1% NaCl (weeks 1, 4, 7), 0% NaCl (weeks 2-3), and 3% NaCl (weeks 5-6) while on a 12:12 light/dark cycle. Subjects were offspring of female Sprague-Dawley rats fed solid chow consisting of either 0.1% (basal), 1% (intermediate), or 3% (high) NaCl throughout pregnancy and lactation. After weaning on postnatal day (PD) 21, offspring were fed the same NaCl diet of their mother until PD 30, at which time all offspring were given Purina 5001 diet (1% NaCl) as their solid chow. On PD 60, 22 adult male offspring (eight basals, six intermediates, eight highs) were implanted with an aortic electronic sensor for transmitting blood-pressure signals by telemetry. MAP and HR varied significantly across the 7-week testing period in association with dietary NaCl levels. The three perinatal salt groups had similar HR levels on normal 1% NaCl chow. However, HR increased in all groups during 0% NaCl and decreased in all groups during 3% NaCl. In contrast, the average MAP levels were significantly greater in the highs compared to both the intermediate and basal groups during both dark and light periods. MAP increased in high and basal groups during both 0% and 3%; however, the increase was more pronounced in the highs. In conclusion, exposure to high levels of dietary NaCl early in development led to a persistent increase in MAP in adulthood.

Animals↗
PubMed2001

NaCl consumption is attenuated in female KCNE1 null mutant mice.

The role of potassium channels in the regulation of NaCl intake has not been investigated previously. One potassium channel, KCNQ1, and its regulator, KCNE1, are expressed in salivary glands and kidneys, and KCNE1 null mutant mice are deficient in KCNQ1 potassium currents. To understand the role of the KCNQ1/KCNE1 channel complex in NaCl taste and intake, we compared the NaCl consumption of KCNE1 +/+ (129/Sv), KCNE1 +/-, and KCNE1 -/- mice using two-bottle intake tests and lick rate tests. Although KCNE1 +/+ and KCNE1 +/- mice exhibited consumption patterns for 75-150 mM NaCl solutions considered typical for 129/Sv mice, the KCNE1 -/- null mutant 129/Sv mice were indifferent to or rejected them. This effect was observed in female mice only, required prior exposure to NaCl solutions, and the extent of rejection was greater after prior exposure to 150 mM NaCl solution than 75 mM NaCl solution. No differences were observed in the avidity for KCl solutions or in lick rates of naive mice for 150 or 300 mM NaCl solutions. These results demonstrate that a single potassium channel gene can influence voluntary NaCl intake. We speculate that disruption of the KCNE1 gene impairs sodium metabolism in female mice drinking high levels of 150 mM NaCl, which causes malaise that becomes associated with NaCl taste, and as a consequence, reduced preference for NaCl.

Animals↗
PubMed1999

The influence of alpha-amanitin on the NaCl-induced up-regulation of antioxidant enzyme activity in cotton callus tissue.

Liquid suspensions of cotton callus tissue from a NaCl-sensitive cell line and a NaCl-tolerant cell line were subjected to the following treatments: (a) 0 and 150 mM NaCl, respectively (controls); (b) 75 and 250 mM NaCl, respectively; (c) 100 ng ml(-1) alpha-amanitin; or (d) pretreatment for 2 h with 100 ng ml(-1) alpha-amanitin followed by the respective NaCl treatments. The callus tissue was harvested at 0, 0.5, 1, 2, 4, and 8h and analyzed for antioxidant enzyme activity. In the NaCl-tolerant callus, the 250 mM NaCl treatment resulted in transient 2- to 4-fold increases above the control levels in the activities of ascorbate peroxidase, catalase, glutathione reductase, and peroxidase within 1 h after treatment, while superoxide dismutase activity increased 4-fold within 4 h. This rapid increase suggests that the up-regulation of antioxidant capacity is an early response to NaCl stress and perhaps provides protection against oxidative damage until other acclimating mechanisms can be invoked. In the control callus, peroxidase activity remained unchanged, and significant increases in the other enzymes were not observed until 8 h after treatment with 75mM NaCl. Pre-treatment with alpha-amanitin prior to the NaCl treatment completely inhibited the NaCl-induced increase in the activities of all five enzymes in both cell lines. This data supports the conclusion that the NaCl-induced up-regulation of antioxidant enzyme activity in cotton callus tissue is transcriptionally regulated, proceeding via a de novo synthesis of poly(A)+RNA and is not due to the translation of existing transcripts or the mobilization of existing enzyme pools. In addition, the results suggest that it is not only the up-regulation of antioxidant activity that bestows a degree of tolerance to environmental stress, but also the speed with which this response occurs.

Amanitins↗
PubMed1988

Exaggerated depressor response to 6-iodoamiloride in NaCl-sensitive spontaneously hypertensive rats.

The current study tested the hypothesis that NaCl-sensitive hypertension may result from increased membrane sodium channel activity. The effect of 6-iodoamiloride, and analog of the sodium channel blocker amiloride, on mean arterial pressure (MAP) was examined in conscious, freely moving NaCl-sensitive spontaneously hypertensive rats (SHR-S) fed high (8%) or normal (1%) NaCl diets. SHR-S and age-matched NaCl-resistant SHR (SHR-R) and normotensive Wistar-Kyoto (WKY) control rats were studied at 9 weeks of age after 2 weeks on either high (8%) NaCl or control (1%) NaCl diets. 6-iodoamiloride was infused intravenously in doses of 0.38 or 0.76 mg/100 g body weight, and MAP and heart rate (HR) were monitored from a femoral arterial cannula for 2 hours. The 8% NaCl diet caused a significant elevation in MAP in SHR-S but not in SHR-R or WKY. Administration of 6-iodoamiloride (both doses) produced a significant, sustained decrease in MAP in both SHR-S and SHR-R. Maximal depressor responses to high dose 6-iodoamiloride were significantly enhanced in SHR-S fed 8% NaCl (31.2 +/- 3.7 mm Hg) compared to SHR-S fed 1% NaCl (14.8 +/- 2.4 mm Hg) or SHR-R fed either 8% or 1% NaCl diets (15.6 +/- 4.2 and 10.2 +/- 3.0 mm Hg, respectively). In contrast, feeding an 8% NaCl diet had no significant effect on the depressor responses to 6-iodoamiloride in either SHR-R or WKY rats. In WKY, these doses of 6-iodoamiloride had no significant effect on MAP in either diet group. 6-iodoamiloride had no significant effect on heart rate in any group. These results support the hypothesis that the exacerbation of hypertension in SHR-S fed a high NaCl diet may result from increased membrane sodium channel activity.

Amiloride↗
PubMed1997

Enhancement of whole cell synaptic currents by low osmolarity and by low [NaCl] in rat hippocampal slices.

We recorded whole cell currents of patch-clamped neurons in stratum pyramidale of CA1 region of rat hippocampal tissue slices. Synaptic currents were evoked by orthodromic stimulation while holding potential of the neuron was varied from hyperpolarized to depolarized levels. Extracellular osmolarity (pi(o)) was lowered by superfusion with artificial cerebrospinal fluid in which NaCl concentration ([NaCl]) was reduced. The effect of low extracellular NaCl was tested in additional trials in which NaCl was substituted by isosmolar fructose. Both lowering of pi(o) and isosmotic lowering of extracellular [NaCl] ([NaCl]o) caused reversible increase of excitatory postsynaptic currents. The effect of lowering pi(o) was concentration dependent, and it was significantly stronger than the effect of equivalent isosmotic lowering of [NaCl]o. Inhibitory postsynaptic currents also increased in many but not in all cases. Lowering of pi(o) caused a prolongation of the time constant of relaxation of the capacitive charging current induced by small hyperpolarizing voltage steps. A virtual input capacitance, calculated by dividing this time constant by the input resistance, increased during hypotonic exposure. Isosmotic lowering of [NaCl]o had no effect on time constant or input capacitance. Depolarizing voltage commands evoked spikelike inward currents presumably representing Na+-dependent action potentials generated outside the voltage-clamped region of the cell. These current spikes became smaller in low pi(o) and in low [NaCl]o. Broader, voltage-dependent, presumably Ca2+-mediated inward currents became more prominent during hypotonic exposure. We conclude that lowering of [NaCl]o causes enhancement of excitatory synaptic transmission. Transmission may be facilitated by the uptake of Ca2+ into presynaptic terminals as well as into postsynaptic target neurons, induced by the low [NaCl]o. Lowering of pi(o) enhances synaptic transmission more than does a corresponding isosmotic lowering of [NaCl]. The excess increase recorded from the cell soma in low pi(o) may in part be due to changing electrotonic length caused by the swelling of dendrites.

Animals↗
PubMed1983

Lack of effect of peritubular protein on passive NaCl transport in the rabbit proximal tubule.

The effect of peritubular protein removal on passive NaCl transport was examined in the isolated rabbit proximal convoluted tubule (PCT). Three modes of passive NaCl transport were tested: (a) paracellular backflux of NaCl, (b) convective flow of NaCl through junctional complexes, and (c) anion gradient-dependent NaCl transport. The effect of peritubular protein removal on the paracellular permeability to NaCl was examined using transepithelial specific resistance. Eight PCT were perfused with ultrafiltrate (UF) and bathed in either serum or UF. Transepithelial specific resistance averaged 14.5 +/- 1.9 in the presence and 13.7 +/- 1.7 omega cm2 in the absence of peritubular protein. The effect of peritubular protein removal on the convective flow of a NaCl solution across functional complexes was examined in the absence of active transport by using colloid osmotic pressure (COP) gradients. 12 PCT were perfused with simple salt solutions in Donnan equilibrium with and without protein at 20 degrees C. A COP gradient of 60.1 and -60.1 mmHg drove only 0.06 and -0.23 nl/min, respectively. These values are approximately 10% of the value predicted for an effect of peritubular protein on NaCl solution flow (1.98 nl/min) and are approximately equal to the value predicted for pure water equilibration for the small osmotic pressure difference between solutions in Donnan equilibrium (0.17-0.18 nl/min). The effect of peritubular protein removal on the passive absorption of NaCl driven by anion concentration gradients was examined in seven PCT perfused with a high chloride solution simulating late proximal tubular fluid and bathed in either serum or UF at 20 degrees C. Volume absorption averaged 0.34 +/- 0.20 in the presence and 0.39 +/- 0.20 nl/mm min in the absence of peritubular protein. In conclusion, peritubular protein removal did not significantly affect any of the three distinct modes of passive NaCl transport tested. The lack of effect of peritubular protein removal on passive paracellular NaCl transport suggests that protein modulates an active transcellular NaCl transport process.

Absorption↗