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PubMed1997

An abnormal sodium metabolism in Japanese patients with essential hypertension, judged by serum sodium distribution, renal function and the renin-aldosterone system.

OBJECTIVE: The role of the renin-aldosterone system and the ability of renal sodium reabsorption to facilitate pressure natriuresis were analyzed by using a sufficient number of Japanese patients with essential hypertension. METHODS: We studied 3222 normal Japanese subjects (610 in Kashiwa City Hospital and 2612 in Shinshu University Hospital), 741 Japanese patients with essential hypertension (256 in Kashiwa City Hospital and 485 in Shinshu University Hospital), 20 patients with aldosterone-producing adenomas and 11 patients with idiopathic hyperaldosteronism to determine the possible roles of sodium, renal function, and plasma aldosterone concentration (PAC) on blood pressure elevation. Inappropriate elevation of aldosterone levels [elevation of the aldosterone:plasma renin activity (PRA) ratio] was used to assess aldosterone action. RESULTS: The peak of the serum sodium distribution curve was approximately 2 mmol/l higher in the patients with essential hypertension than it was in controls. The prevalence of higher serum sodium concentrations (> or = 147 mmol/l) also was increased significantly hypertensive patients. Age-related deterioration of renal function did not explain the hypertension and abnormal sodium metabolism in the hypertensive patients. In stepwise regression analysis, the serum sodium concentration was related inversely to the PRA and positively to the PAC:PRA ratio. Although there was an inverse relationship between urinary sodium excretion (representing sodium intake) and the PRA, urinary sodium excretion proved not to be significant as a source of variation in the PAC or in the PAC:PRA ratio in the hypertensive patients. Although the PAC was within the normal range in patients with serum sodium concentrations of 147 mmol/l or more and an elevated PAC:PRA ratio, it was inappropriately high for the stimulus applied, as indicated by the PRA; this is similar to the situation with aldosterone-producing adenomas or idiopathic hyperaldosteronism. CONCLUSION: Serum sodium distribution patterns differed between normal subjects and patients with essential hypertension in this Japanese population. The deterioration of renal function and increased sodium intake did not explain this abnormal sodium metabolism. A higher serum sodium concentration is related to an elevated blood pressure, and, in some patients, an inappropriate elevation of plasma aldosterone levels. Of the Japanese hypertensive patients, 10-14% exhibited serum sodium concentrations of 147 mmol/l or more and inappropriate elevations of aldosterone level (suppressed PRA and normal aldosterone level). The defect in these patients presumably lies in the inappropriately high secretion of aldosterone.

Adult↗
PubMed1977

Sodium chloride transport across the chicken coprodeum. Basic characteristics and dependence on sodium chloride intake.

1. The transport characteristics of the chicken coprodeum have been examined in vitro using the isolated mucosa. The short-circuit current (I(sc)), the transepithelial electrical potential difference (p.d.), the unidirectional transmural fluxes (J(ms), J(sm)) of sodium and chloride measured in the short-circuited state, and the unidirectional influx of sodium and chloride across the brush border membrane measured under open-circuit conditions have been studied. The effect of the sodium chloride contents of the diet on these parameters have been investigated.2. The isolated mucosa depends functionally on the presence of glucose in the incubation media. This dependence reflects the need of glucose as a fuel. There is no indication of coupling between transport of sugars and sodium across the brush border membrane. For preparations from chickens on a low sodium diet a very high and stable I(sc) can quantitatively be accounted for by the net transport of sodium. Influx of sodium across the brush border membrane is not significantly different from the net flux of sodium. By feeding the chickens a high sodium diet the I(sc) is reduced by more than 95%, the net transport of sodium is abolished, and the transepithelial electrical conductance is reduced by more than 50%.3. Both unidirectional transepithelial fluxes of chloride, and the serosa to mucosa flux of sodium appear to proceed through a paracellular shunt.4. Under the conditions of the low sodium diet the paracellular pathway appears to be anion selective. Whereas, under the conditions of the high sodium regimen the paracellular route appears to be cation selective. After adaptation to a high sodium diet the influx of sodium across the brush border membrane is only moderately reduced. Consequently the decisive event in the adaptation must be localized elsewhere.

Animals↗
PubMed1982

Sodium currents and sodium-current fluctuations in rat myelinated nerve fibres.

1. Sodium currents and fluctuations of sodium currents were measured in myelinated fibres of rat sciatic nerve under voltage clamp at 20 degrees C.2. Relaxations of sodium currents during various test potentials were recorded in the presence of 6 nM-TTX in the extracellular solution. The activation of sodium currents at low depolarizations could be described with the m(2) formulation. At increasing potentials higher powers of m up to 4 were required. The mid-point of the P(Na) (E) curve was located near E = -32 mV. Sodium inactivation during various depolarizations developed in two phases.3. The resistance in series with the nodal membrane was calculated from peak sodium currents without and with 6 nM-TTX in the extracellular solution. The resistance varied between different fibres and ranged between 190 and 620 kOmega.4. From peak sodium currents at the same mambrane potential without and in the presence of TTX an apparent equilibrium dissociation constant of 1.6 nM was calculated for TTX binding to sodium channels.5. The conductance gamma and the number N(0) (corrected for series-resistance effects) of sodium channels were evaluated from ensemble average values of the mean sodium current and the variance of sodium-current fluctuations at the beginning of a test pulse. The mean values were gamma = 14.5 pS, N(0) = 21,000 per node.6. The spectral density of stationary sodium-current fluctuations exhibited two relaxation components whose time constants were comparable to those of sodium activation and inactivation. At low depolarizations the variance produced by inactivation fluctuations was larger than predicted by the m(3). h formulation.7. It is concluded that individual sodium channels of rat and frog nerve have similar gating properties. In mammalian nodes the number of sodium channels is lower and the single-channel conductance higher than in amphibian nodes.

Action Potentials↗
PubMed1985

Sodium pump inhibition, enhanced calcium influx via sodium-calcium exchange, and positive inotropic response in cultured heart cells.

The effects of sodium pump inhibition produced by exposure to the cardiac glycosides, ouabain or dihydroouabain, or by reduction in extracellular potassium to 1.0 mM, on contractile state and sodium-calcium exchange were studied in primary monolayer cultures of chick embryo ventricular cells. Ouabain, 10(-6)M, dihydroouabain, 5 X 10(-5)M, and extracellular potassium of 1.0 mM all induced similar and prominent positive inotropic effects. These effects were accompanied, in each case, by 40-50% inhibition of the rate of active uptake of 42K and by similar increases in steady state sodium content. Stimulation of the rate of 45Ca uptake on exposure to zero extracellular sodium occurred in response to extracellular potassium (1.0 mM) or to glycoside concentrations that induced a positive inotropic effect and sodium-potassium pump inhibition. Reactivation of the sodium pump after return from 1.0 to 4.0 mM extracellular potassium was rapid and was associated with membrane hyperpolarization and slowing of spontaneous beating rate. With pump reactivation under these circumstances, the time course of disappearance of stimulation of sodium-calcium exchange on exposure to zero extracellular sodium was similar to the time course of loss of the positive inotropic effect. Under physiological conditions (4.0 mM extracellular potassium), exposure to positively inotropic but nontoxic concentrations of ouabain or dihydroouabain caused a small but consistent increase in unidirectional calcium influx, but had no discernible effect on calcium efflux. Since similar inotropic effects were produced for comparable degrees of glycoside or low extracellular potassium-induced sodium pump inhibition and increases in cellular sodium content, sodium pump inhibition rather than a glycoside-specific change in calcium binding appears to underlie the inotropic response. These findings are further consistent with the view that the primary mechanism of the positive inotropic effects of digitalis and low extracellular potassium in this experimental preparation is sodium pump inhibition resulting in increased intracellular sodium. We suggest that increased calcium influx via sodium-calcium exchange is the principal mechanism whereby increased intracellular sodium results in enhanced calcium availability to the myofibrils, but an additional effect on calcium efflux is not excluded.

Animals↗
PubMed1978

Kinetics of the co-transport of phenylalanine and sodium ions in the guinea-pig small intestine. II. Sodium fluxes and flux ratios.

The validity of a general non-compulsory model for the description of the co-transport of sodium and phenylalanine in the small intestinal mucosa of the guinea-pig has been examined by measuring the influx of sodium and the flux ratios. The simultaneous influxes of sodium and phenylalanine have been determined by incubating intestinal tissues at a fixed sodium and variable phenylalanine concentrations. The experiment was repeated at a number of sodium concentrations, and a straight-line relationship between the fluxes was always obtained. The slope of this line, the flux ratio, is dependent on the sodium concentration; the function is biphasic inasmuch as it rises with sodium concentration at low external sodium, but decreases when the sodium concentration is raised above a level of about 70 mM. This response is compatible with the model under examination. No saturable component of sodium influx could be detected in the absence of phenylalanine, but the values of this influx corresponded with those predicted from the flux ratio experiment. In the presence of phenylalanine, sodium influx could be resolved into saturable and non-saturable components, and the Kt for sodium influx via the saturable mechanism agreed with that predicted from the constants derived from measurements of phenylalanine influx. The maximal velocity for sodium influx was similar to the maximal velocity for phenylalaline influx. Equations were derived to examine the behaviour of sodium influx as a function of the external phenylalanine concentration, and a Kt for phenylalanine was deduced which agrees closely with that obtained by studying phenylalanine fluxes directly. These results provide evidence in favour the applicability, in this species, of a model involving no compulsory pathway for the formation of a ternary complex between the carrier, a sodium ion and the phenylalanine molecule. Examination of the literature suggests that in other species different models may describe more accurately this co-transport mechanism.

Animals↗
PubMed1996

Heterogeneous patterns of sodium excretion during sodium restriction in essential hypertensive patients.

OBJECTIVE: To study the sodium excretory pattern by which sodium balance is reached. METHODS: Ninety untreated essential hypertensives with a median age of 47 (range: 18-70 years) were admitted to a metabolic ward for 7 days and put on a sodium diet of 55 mmol/day. During these 7 days urinary excretions of sodium, potassium and creatinine were determined daily along with mean arterial pressure (MAP) and weight. RESULTS: Changes in urinary sodium excretion were not uniform, but according to the pattern of attaining sodium balance, subjects could be divided into four groups. Group 1 (n = 31) gradually reached sodium balance, whereas group 2 (n = 10) showed an abrupt fall in sodium excretion on the third day and an extremely fluctuating sodium excretion thereafter. Group 3 (n = 32) reached sodium balance on day four, but displayed a rise in sodium excretion during the following days and group 4 (n = 17) attained sodium balance only very slowly or not at all. Compared to the other groups, group 4 lost more sodium and at the same time displayed a greater fall in blood pressure. CONCLUSIONS: Our data suggest that there may be at least four different patterns by which sodium balance can be reached following a reduction in sodium intake. The determinants of these responses remain, however, elusive.

Adolescent↗
PubMed1994

Dietary sodium intake, airway responsiveness, and cellular sodium transport.

Both epidemiologic and experimental evidence suggest that a high dietary sodium intake may increase airway responsiveness, but no adequate explanation exists of how changes in sodium intake might lead to increased responsiveness. This investigation was carried out to study dietary sodium intake and airway response to methacholine in relation to cellular sodium transport in 52 young men. Airway response to methacholine was associated with urinary sodium excretion when subjects were on normal sodium intake. Airway responsiveness in patients with mild asthma correlated with the furosemide-insensitive influx of sodium into peripheral leukocytes stimulated by autologous serum, but there was no relation between this influx and 24-h urinary sodium excretion. In a separate investigation, serum from subjects with increased airway responsiveness caused an increase in the sodium influx and sodium content of leukocytes from nonatopic subjects. The magnitude of the furosemide-insensitive, serum stimulated influx was related to the degree of airway responsiveness of the serum donor, as was the increase in intracellular sodium content. Neither was related to the 24-h urinary sodium excretion of the donor. Patients with airway hyperresponsiveness have an increased sodium influx into cells stimulated by a serum-borne factor. This is independent of the effect of added dietary sodium on airway responsiveness.

Adolescent↗
PubMed1990

Distal lithium reabsorption in the sodium-restricted rat is not dependent on the urinary sodium to lithium concentration ratio.

1. High fractional reabsorption of lithium occurs when rats and dogs are given a low sodium diet. This has been suggested to be due to the low tubular fluid sodium to lithium concentration ratio which arises during sodium restriction allowing transport mechanisms along the distal nephron segment to accept significant quantities of lithium instead of sodium by simple competition. 2. Clearance experiments in conscious water-loaded Wistar rats maintained on either a low sodium (6 mmol/kg) or a normal sodium (120 mmol/kg) diet were performed. The rats were infused with a solution of 120 mmol/l glucose and 10 mmol/l NaCl at a rate of 6 ml/h. 3. The median fractional excretion of lithium was 19.4% in the group with a normal sodium intake, and 2.5% in the group given a low sodium diet. The urine to plasma concentration ratio of lithium was 2.5 in the normal sodium group and 0.4 in the sodium-restricted group. The urinary sodium to lithium concentration ratio was 13 in the control group and 63 in the sodium-restricted group. 4. It is concluded that the increased fractional reabsorption of lithium initiated by a low sodium intake is not likely to be due to simple competition at distal tubular nephron sites between lithium and sodium.

Absorption↗
PubMed2001

Sodium homeostasis with chronic sodium loading in preascitic cirrhosis.

BACKGROUND: Preascitic cirrhotic patients receiving 200 mmol of sodium daily for seven days remain in positive sodium balance. Thereafter, sodium handling is unknown. AIM: To assess renal sodium handling in preascitic cirrhosis on a high sodium diet for five weeks. METHODS: Sixteen biopsy proven preascitic cirrhotics were assessed at weekly intervals for five weeks on a diet of 200 mmol sodium/day using a daily weight diary and weekly 24 hour urinary sodium estimations. Fasting supine neurohormone levels were measured at baseline and weekly for five weeks while haemodynamics were measured at baseline and at five weeks. RESULTS: The daily diet of 200 mmol of sodium resulted in weight gain and a positive sodium balance for three weeks, associated with significant suppression of plasma renin activity and aldosterone levels, and a significant rise in plasma atrial natriuretic peptide levels (p<0.05). Patients' weights plateaued during week 4, associated with complete sodium balance and significant suppression of plasma noradrenaline levels (p<0.05). This was followed by a negative sodium balance and weight loss, and finally complete sodium balance, again despite a mean net gain of 2.3 (0.3) kg, associated with a return of plasma renin activity and aldosterone levels to within normal ranges. The lack of increase in central blood volume in addition to the persistent increase in plasma atrial natriuretic peptide levels indicated that residual volume expansion, consequent to persistent weight gain, was distributed on the venous side of the circulation. No free fluid was seen on repeat abdominal ultrasound after five weeks. CONCLUSION: Preascitic cirrhotics have a natriuretic "escape" after three weeks on high sodium dietary intake, associated with elevated plasma atrial natriuretic peptide levels and suppression of the renin-angiotensin-aldosterone system. With continued suppressed sympathetic activity, preascitics re-establish complete sodium balance but with a net weight gain and presumed increased intravascular volume, but without ascites. This further elucidates the compensated sodium retaining abnormality that characterises preascitic cirrhosis.

Aldosterone↗
PubMedDate not supplied

Rat thymocyte sodium transport. Effects of changes in sodium balance and experimental hypertension.

The wide range of membrane electrolyte transport abnormalities associated with experimental, genetic, and essential hypertension may either reflect an underlying global change in the cell membrane or may be directly related to the underlying disturbance that causes hypertension or to changes in sodium balance. To investigate this further, we studied sodium transport and intracellular electrolyte composition in the thymocytes of normal rats undergoing salt loading or depletion, and in rats with renovascular, mineralocorticoid, or spontaneous hypertension compared to appropriate age-matched normotensive control rats. In normotensive rats, although there was no significant difference between the blood pressures at the two extremes of sodium balance, sodium loading caused a nonsignificant rise in sodium transport, whereas sodium depletion was associated with a significant fall in sodium transport and intracellular sodium. When cells from salt-loaded or normal animals were incubated in a medium containing their own serum, sodium transport was slightly stimulated in both, but there was no significant difference in the sodium efflux-rate constant of thymocytes obtained from rats on the normal as opposed to the high salt intake. Compared to normotensive rats, there was no significant change in the sodium efflux-rate constant in any of the hypertensive rat models studied. However, the sodium efflux-rate constant fell with age in both the spontaneously hypertensive and Wistar-Kyoto normotensive rats. The present studies show that dietary sodium intake and aging had considerable effects on rat thymocyte sodium transport, but neither of these changes was related to a change in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Inhibition of nonproteolytic, psychrotrophic clostridia and anaerobic sporeformers by sodium diacetate and sodium lactate in cook-in-bag turkey breast.

A nonproteolytic, psychrotrophic Clostridium isolate, designated strain OMFRI1, was recovered from cook-in-bag turkey breasts (CIBTB) that displayed an intense pink discoloration and an off-odor following extended refrigerated storage. The viability of strain OMFRI1 in CIBTB containing sodium diacetate (at 0, 0.25, and 0.5%) and/or sodium lactate (at 0, 1.25, and 2.5%) was subsequently evaluated. Raw CIBTB batter was inoculated with 9 to 30 spores of strain OMFRI1 per g, vacuum packaged, cooked to an instantaneous internal temperature of 71.1 degrees C, chilled, and incubated at 4 degrees C for up to 22 weeks. In the absence of food-grade antimicrobial agents, spoilage (i.e., an off-odor) occurred within 6 weeks, and anaerobic plate counts reached 6.6 log10 CFU/g. The CIBTB containing sodium diacetate (0.25%) and that containing sodium lactate (1.25%) required 12 weeks for spoilage to occur and for anaerobic plate counts to reach 7.0 and 6.0 log10 CFU/g, respectively. When sodium diacetate (0.25%) and sodium lactate (1.25%) were used in combination, no off-odor was detected and anaerobic plate counts did not exceed 2.3 log10 CFU/g over 22 weeks of storage at 4 degrees C. In related experiments, sodium diacetate (at 0, 0.25, and 0.5%), sodium lactate (at 0, 1.25, and 2.5%), and combinations of both ingredients were evaluated in uninoculated CIBTB incubated at 25 degrees C for up to 22 days. In the absence of antimicrobial agents and in CIBTB containing sodium diacetate (0.5%), spoilage occurred within 8 days and anaerobic plate counts reached 6.8 and 6.6 log10 CFU/g, respectively. Samples of CIBTB containing sodium lactate (2.5%) showed signs of spoilage within 22 days, and anaerobic plate counts for these samples ranged from < or = 1.0 to 6.3 log10 CFU/g. In CIBTB containing both sodium lactate (2.5%) and sodium diacetate (0.25%), spoilage was not evident and anaerobic plate counts were < or = 1.0 log10 CFU/g within 22 days. These data validate the efficacy of sodium lactate and sodium diacetate in extending the shelf life of CIBTB.

Animals↗
PubMed1978

Sodium exchange between two sites. The binding of sodium to halotolerant bacteria.

The longitudinal and transverse relaxation curves of sodium undergoing exchange between two sites are presented. When the two sites are 'bound' and 'free' sodium respectively, the relaxation curves are, in general, not exponential. It is shown that in some cases only one exponential decay could be detected experimentally though the true decay curve is much more complicated. In such cases where the population of 'free' and 'bound' sodium are equal, only 40-70% of the total intensity would be detected, depending on the lifetime of sodium in the two sites. It is also shown that the fast exchange approximation, usually applied in the interpretation of sodium relaxation curves, might lead to wrong conclusions. Measurements of sodium relaxation times in halotolerant bacteria show that T1 and T2 are different and frequency-dependent. The intensity of the sodium sugnal is 40% of the total sodium concentration. It was possible to simulate the relaxation behaviour and intensity measurements by applying the following model. There are three types of sodium, the extracellular sodium (A) which exchanges with part of the intracellular sodium (B) and a fraction (C) which is bound but does not exchange with the extracellular sodium. It was possible to estimate the physical properties of sodium at site B. The quadrupole coupling constant (e2qQ/H)B = 9.10(6) rad/s, the correlation time taucB = 5.5.10(-7) s and the lifetime of sodium at site B, tauB = 6.10(-4) s.

Bacteria↗
PubMed1997

Activation of sodium transport and intracellular sodium lowering by the neuroleptic drug chlorpromazine.

Chlorpromazine (CPZ), a commonly used antipsychotic drug, at high concentration was found to reduce significantly the sodium content of both rat (Rattus norvegicus) and toad (Bufo marinus) liver cells. This reduction in intracellular sodium was demonstrated using 22Na+ flux and measurement of cell sodium content. The results suggest that the sodium-lowering effect of CPZ stemmed from a stimulation of sodium transport rather than from an inhibition of sodium influx (i.e., sodium channels), cell damage, or Na+:Na+ exchange. CPZ was found to interfere with the binding of ouabain to the sodium pump, although a simple reduction in sodium pump inhibition did not account for the sodium-lowering effect. CPZ was able to negate the effects of monensin, a sodium ionophore, suggesting a substantial capacity to activate sodium transport. The intracellular sodium-lowering action of CPZ through the activation of sodium transport represents a new property previously undescribed for this drug.

Animals↗
PubMed1967

The sensitivity of the sodium pump to external sodium.

1. When red cells are incubated in potassium-free solutions, ouabain-sensitive sodium efflux is nearly absent with 5 mM-Na externally, but increases as the external sodium concentration is reduced from 5 mM to zero. This increase suggests that the transport mechanism is very sensitive to small amounts of sodium at the outside surface of the cell membrane. Further evidence for such sensitivity has been obtained from the effects of external sodium on the relation between potassium influx and external potassium concentration.2. With 5 mM-[K](o), potassium influx is rather insensitive to [Na](o) but at low potassium concentrations even low levels of sodium inhibit.3. With 140 mM-[Na](o) the potassium influx curve is S-shaped below 1 mM [K](o). At much lower sodium concentrations, the S-shaped region and the value of [K](o) for which potassium influx is half-maximal are both shifted progressively towards zero. At 10 muM-[Na](o), potassium influx is half maximal at 0.14 mM-[K](o) and the curve is close to a rectangular hyperbola down to 22 muM-[K](o); there seems to be a trace of inflexion at about 15 muM-[K](o).4. When [Na](o) is reduced from 5 mM to zero, removal of the inhibitory effect of external sodium ions on sodium: potassium exchange could lead to an increase in sodium efflux into nominally potassium-free solutions if these solutions did in fact contain traces of potassium. Such traces could arise by leakage from the cells, but, in a number of experiments, direct measurements showed that [K](o) was too low to account in this way for all of the observed ouabain-sensitive sodium efflux. A further reason for rejecting this explanation is that ouabain-sensitive potassium loss into nominally (Na+K)-free solutions was unaffected by adding 5 mM-Na. (A slight increase in ouabain-resistant loss was observed.)5. The ouabain-sensitive efflux of sodium into (Na+K)-free solutions therefore seems to represent a mode of behaviour of the transport mechanism distinct both from the sodium: potassium exchange that occurs under physiological conditions and from the sodium: sodium exchange that occurs in K-free, Na-rich media.

Biological Transport↗
PubMedDate not supplied

The biliary and urinary excretion of sodium tyropanoate and sodium ipodate in dogs: pharmacokinetics, influence of bile salts and choleretic effects with comparison to iopanoic acid.

The biliary and urinary excretion of sodium tyropanoate (Bilopaque) and sodium ipodate (Oragrafin) were studied in unanesthetized bile-fistula dogs using stepwise, increasing, intravenous infusions of the contrast materials. A constant intravenous infusion of sodium taurocholate was administered at the rate of either 0.5 or 2.0 mu moles per min per kg throughout each experiment. The biliary excretion of sodium tyropanoate or sodium ipodate was not effected by the rate of sodium taurocholate infusion. The maximum rate of biliary excretion of sodium ipodate was significantly greater than that of sodium tyropanoate with the low taurocholate infusion, but there was no significant difference between the two with the high taurocholate infusion. With the low taurocholate infusion the maximum biliary excretion rate of sodium tyropanoate (0.956 mu moles per min per kg) and sodium ipodate (1.472 mu moles per min per kg) were significantly greater than the maximum biliary excretion of iopanoic acid (Telepaque) (0.671 mu moles per min per kg). With the high taurocholate infusion the maximum biliary excretion rates of the three contrast agents were not statistically different. Both sodium tyropanoate and sodium ipodate produced an increase in canalicular bile flow (8-11 ml per millimole). These data suggest that in clinical cholecystography sodium tyropanoate and sodium ipodate are not excreted in bile more rapidly than iopanoic acid, except when the rate of biliary excretion of bile salts is low; that is, except in patients who are fasting or those who are on a fat-free diet.

Animals↗
PubMed1984

The dual effect of sodium ion on the digitalis-sodium pump interaction.

Digitalis glycosides are specific inhibitors of the sodium pump. While their effects on isolated Na,K-ATPase, an enzymatic representation of the sodium pump, can be quantified easily and precisely, estimation of their effects on the sodium pump and evaluation of the physiological significance of sodium pump inhibition are complicated by several factors. In isolated Na,K-ATPase, the specific binding of cardiac glycosides observed in the presence of Mg2+ and ATP is stimulated by Na+. In intact myocardial cells, conditions which enhance Na+ influx, and hence the amount of Na+ to be transported by the sodium pump, such as stimulation at high frequencies, presence of monensin (a sodium ionophore), batrachotoxin or grayanotoxin I, enhance the glycoside binding to the sodium pump. In left atrial muscle preparations isolated from the guinea-pig heart and stimulated at 0.5 Hz, binding of ouabain to glycoside binding sites on Na,K-ATPase was eliminated by lowering the extracellular Na+ concentration from 145 to 27 mM, a condition reported to lower the intracellular Na+ concentration by more than 60%. When ouabain exposure of atrial muscle preparations was restricted to the quiescent period, glycoside binding to the sodium pump was minimal. Monensin, however, caused ouabain to bind to the sodium pump in quiescent preparations. These results indicate that glycoside binding to the sodium pump is enhanced by intracellular Na+. In addition to enhancing the glycoside binding to the sodium pump, an elevation of intracellular Na+ reduces the reserve capacity of the sodium pump and therefore increases the sensitivity of the myocardium to sodium pump inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effects of sodium bicarbonate and sodium chloride on the elimination of etorphine in equine urine.

The combination of large doses of sodium bicarbonate and the potent narcotic, etorphine, has reportedly been given to racehorses in attempts to improve their performance and also to "mask" the presence of etorphine in urine samples. The increased urinary output and pH associated with sodium bicarbonate (approximately 500 g) administration may reduce the urinary concentration of etorphine, making it more difficult to detect. Our experiment was designed to examine the effects of this combination. Six Thoroughbred horses were used in a latin-square design with three horse pairs and three treatments consisting of the following: etorphine (20 micrograms), etorphine (20 micrograms) plus sodium bicarbonate (1.0 g/kg), and etorphine (20 micrograms) plus sodium chloride (0.7 g/kg). Sodium chloride was used to distinguish between the urinary alkalinizing effects of sodium bicarbonate and the diuretic effects associated with the large electrolyte load. Venous blood and urine samples were collected prior to and for 24 h post-treatment. Sodium bicarbonate produced a significant metabolic alkalosis and an increase in urine pH. Both sodium bicarbonate and sodium chloride produced a profound diuresis. After sodium bicarbonate and sodium chloride treatments, the urinary concentration of etorphine, measured by radioimmunoassay (RIA), was reduced and in some cases could not be detected. Extraction of the urine samples, prior to RIA analysis, increased the sensitivity of the assay and in most cases gave a positive result. We conclude that the coadministration of etorphine and sodium bicarbonate or sodium chloride can make the detection of etorphine more difficult because of the dilutional effects associated with the administration of a large electrolyte load.

Animals↗
PubMed1995

Glomerular function and structure in the sodium-replete and sodium-deplete uninephrectomized spontaneously hypertensive rat: effect of blood pressure reduction, glomerular structure, and blood pressure reduction.

To assess the effects of chronic dietary sodium restriction and blood pressure reduction on glomerular function and structure during the pathogenesis of hypertensive renal disease, experiments were conducted in uninephrectomized (UNX) spontaneously hypertensive rats (SHR) using the dihydropyridine calcium antagonist manidipine. Male SHRs underwent UNX at age 10-11 weeks and subsequently were assigned to one of four groups: sodium-replete (0.4%); sodium-replete and a predetermined antihypertensive dose of manidipine (20 mg/kg body weight); sodium-deplete (0.09%); and sodium-deplete and manidipine (20 mg/kg body weight). Twelve weeks later, renal morphologic and functional studies were performed. Sodium restriction had no significant effect on systolic blood pressure, but creatinine clearance and urinary protein excretion were decreased. Importantly, mean glomerular volume and the prevalence of mesangial expansion were lower with sodium restriction. This occurred in the presence of high concentrations of plasma and renal tissue angiotensin II. Manidipine significantly reduced systolic blood pressure in the sodium-replete and sodium-deplete UNX-SHRs. This therapy was not associated with significant changes in creatinine clearance and urinary protein excretion in the sodium-deplete or sodium-replete UNX-SHRs. The prevalence of mesangial expansion in the sodium-replete UNX-SHR was approximately 50% lower with manidipine. Plasma and renal tissue angiotensin II concentrations were not affected by the drug. In the sodium-deplete UNX-SHR, the prevalence of mesangial expansion was not reduced further by manidipine. However, plasma and renal tissue angiotensin II concentrations were increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗