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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cloned human embryonal carcinoma cells (NTERA-2 cl.D1) differentiate into neuron-like cells upon exposure to retinoic acid. Using whole-cell patch-clamp techniques, these putative neurons exhibited rapidly activating and inactivating inward currents upon depolarization as well as outward currents. The electrical characteristics and tetrodotoxin (TTX) sensitivity of the inward currents suggest that they were sodium currents. By contrast, only outward potassium currents were seen in the undifferentiated stem cells. Under current clamp conditions, the neuron-like cells showed regenerative responses. The peaks of these responses never exceeded the O-mV level, perhaps due to the low mean inward current density of 93.8 +/- 17.8 (SEM) microA/cm2:n = 9. The electrophysiological characteristics of these human teratocarcinoma-derived neuron-like cells were consistent with our previous identification of these cells as neurons, but suggest that they may resemble immature embryonic, rather than adult, neurons.
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PMID:Presumptive neurons derived by differentiation of a human embryonal carcinoma cell line exhibit tetrodotoxin-sensitive sodium currents and the capacity for regenerative responses. 253 15

The relationship between erythrocyte Na,K-ATPase activity (ouabain-inhibited 86Rb uptake) and metabolic efficiency (defined as the resting metabolic rate adjusted for body composition) was examined in 31 healthy young subjects (16 men and 15 women, 19-33 yr old). Mean (+/- SEM) Na,K-ATPase activity (expressed as nanomoles of Rb taken up per h/billion erythrocytes) was similar in the men (86 +/- 3) and women (94 +/- 7). After adjusting metabolic rate for body cell mass (total body potassium), men and women had similar metabolic rates, and subjects with the highest percent body fat tended to have the highest metabolic rates. Ouabain-sensitive erythrocyte Rb uptake was related to less than 2% of the variability in resting metabolic rate after adjusting metabolic rate for differences in body composition. Erythrocyte Na,K-ATPase activity does not appear to be a useful marker of metabolic efficiency in man.
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PMID:No correlation between erythrocyte Na,K-ATPase activity and resting metabolic rate in humans. 255 May 12

Terbutaline, a beta 2-adrenergic agonist, has been shown to cause hypokalemia and an increase of plasma glucose and serum insulin concentrations. We considered that terbutaline-induced hypokalemia may be due to the insulin-induced shift of potassium (K+) from the extracellular to the intracellular space. If so, then inhibition of insulin secretion by somatostatin would prevent terbutaline-induced hypokalemia. Further, we wondered whether oral potassium pretreatment could prevent terbutaline-induced hypokalemia. Therefore, 10 healthy volunteers (5 men, 5 women; mean age, 23 yr +/- 3 SD) received either sodium chloride (NaCl) or somatostatin intravenously together with 0.25 mg terbutaline subcutaneously in a double-blind crossover design. On a third test day, they received 39 mval of K+ powder orally before terbutaline injection in an open trial. Terbutaline caused a significant decrease of K+ (from 3.96 +/- 0.08 to 3.3 +/- 0.13 mmol/L +/- SEM; p less than 0.0005), accompanied by a significant increase in plasma glucose (from 83 +/- 3.6 to 101 +/- 4.4 mg/dl +/- SEM; p less than 0.01) and serum insulin concentrations (from 11.7 +/- 0.9 to 19.9 +/- 1.1 microU/ml +/- SEM; p less than 0.001), confirming earlier data. Somatostatin pretreatment inhibited the terbutaline-induced hypokalemia; the small fall of K+ (from 3.7 +/- 0.08 to 3.5 +/- 0.2 mmol/L) was no longer significant. Insulin secretion was completely blocked by somatostatin, leading to an even more pronounced increase of blood glucose. Hypokalemia after terbutaline injection was not prevented by oral potassium pretreatment. In summary, the present findings confirm that terbutaline-induced hypokalemia is associated with increased plasma glucose and insulin levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of somatostatin and oral potassium administration on terbutaline-induced hypokalemia. 256 17

111 untreated subjects (mean [SEM] age 58.4 [1.0] years; 93 male, 18 female) with diastolic blood pressure between 90 and 100 mm Hg were seen fortnightly, and after four pre-diet visits they were randomised into a low sodium intake group (53 subjects; diet containing less than 80 mmol sodium/day plus 8 placebo tablets daily) or a normal sodium intake group (55 subjects; same dietary sodium plus 8 slow-release sodium chloride [10 mmol] tablets daily). 103 subjects completed the intervention phase of 8 weeks. Urinary sodium fell significantly in the low sodium group but not in the normal sodium group. Urinary potassium excretion did not change in either group. Mean (SEM) systolic and diastolic blood pressure fell by 6.1 (1.1) and 3.7 (0.6) mm Hg, respectively, in the low sodium group, but by only 0.6 (1.0) and 0.9 (0.6) mm Hg in the normal sodium group. Multivariate analysis allowing for the effects of pre-diet blood pressure, weight, and age, reduced the effect of lowering the sodium intake on the systolic pressure from 5.5 (SEM 1.5) mm Hg to 4.8 (1.3) mm Hg (p less than 0.005) but the effect on diastolic pressure was not changed significantly.
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PMID:Fall in blood pressure with modest reduction in dietary salt intake in mild hypertension. Australian National Health and Medical Research Council Dietary Salt Study Management Committee. 256 8

The effects of low bolus dose (70 +/- 6 micrograms [mean +/- SEM]) atrial natriuretic factor (ANF) administration was assessed in 16 patients with chronic congestive heart failure. Measurements were made for at least 60 minutes before and after the dose of ANF. There was a significant increase in urine flow rate (0.81 +/- 0.06 to 1.81 +/- 0.23 ml/min, p less than 0.01), sodium excretion rate (56 +/- 14 to 80 +/- 23 microEq/min, p less than 0.01), fractional excretion of sodium (1.23 +/- 0.49 to 1.63 +/- 0.60 percent, p less than 0.01) and potassium excretion rate (35 +/- 7 to 42 +/- 6 microEq/min, p less than 0.02). However, no significant alterations in renal plasma flow or glomerular filtration rate were observed. Furthermore, there was no significant correlation between the change in urine flow rate or sodium excretion rate and the change in renal plasma flow or glomerular filtration rate, respectively. In addition, there was no significant effect on cardiac index, mean aortic or left ventricular filling pressures, or systemic vascular resistance. There also was no discernible relationship between the response to ANF and the baseline concentrations of plasma ANF, aldosterone, or plasma renin activity. Thus, in patients with congestive heart failure, low dose ANF boluses may produce an increase in urine flow rate and sodium excretion rate that is independent of renal plasma flow or glomerular filtration rate. This suggests a meaningful direct renal tubular effect of exogenous ANF in this setting.
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PMID:Cardiorenal effects of atrial natriuretic factor administration in congestive heart failure: natriuresis and diuresis without hemodynamic alterations. 256 86

Free cytosolic calcium concentration, [Ca2+]i, in single rat pituitary cells can be measured with the fluorescent, calcium-sensitive probe fura-2 and digital image analysis. A reverse hemolytic plaque assay (RHPA) identifies somatotropes in the mixed population of pituitary cells. Previous studies showed that growth hormone releasing factor (GRF) stimulates growth hormone (GH) release from pituitary somatotropes by increasing the influx of calcium into the cell. Somatostatin reduced [Ca2+]i and inhibits hormone release presumably by closing calcium channels in the membrane. The calcium-ionophore bromo-A23187 rapidly increased [Ca2+]i from a baseline of 226 +/- 38 nM to a peak of 842 +/- 169 nM (mean +/- SEM) which was reached 30 s after exposure to the drug. This spike was followed by a sustained phase of elevated [Ca2+]i approximately 370 nM. When somatostatin (SRIF) (10 nM) was combined with ionophore treatment, the initial rise was preserved. However, the second phase was abolished and SRIF lowered [Ca2+]i to 57 +/- 7 nM. Depolarizing the cellular membrane with high extracellular potassium (60 mM) increased cytosolic calcium as well (797 +/- 178 nM); however, this was not affected by the addition of SRIF (988 +/- 71 nM). KCl depolarization in calcium-free medium (+1.5 mM EGTA) provoked no rise in cytosolic calcium. In contrast, after ionophore, the initial spike was preserved while the sustained phase of elevated [Ca2+]i was abolished. We conclude from these data that (1) membrane depolarization and ionophore treatment lead to an influx of calcium into the cytosol of normal pituitary somatotropes. (2) SRIF inhibits calcium influx induced by ionophore but not influx after depolarization with high potassium concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ionophore bromo-A23187 reveals cellular calcium stores in single pituitary somatotropes. 256 28

Epidemiologic studies suggest an inverse relation between potassium intake and the prevalence of hypertension. To investigate the effect of dietary potassium restriction on blood pressure, we used a randomized crossover design to study 10 healthy, normotensive men randomly assigned to isocaloric diets (each lasting nine days) providing either low (10 mmol per day) or normal (90 mmol per day) amounts of potassium, while sodium intake was maintained at the subjects' usual levels (120 to 200 mmol per day). With the low-potassium diet, plasma potassium levels declined from 3.8 to 3.2 mmol per liter (P less than 0.001), but plasma sodium and chloride levels were unchanged. The average daily excretion of urinary sodium (+/- SEM) on the low-potassium diet was significantly lower than that with the normal-potassium diet (10 +/- 10 vs. 144 +/- 10 mmol; P less than 0.001). The mean arterial pressure did not change significantly during normal potassium intake, but it increased over the nine days of the low-potassium diet from 90.9 +/- 2.2 to 95.0 +/- 2.2 mm Hg (P less than 0.05). Both mean arterial (P less than 0.01) and diastolic (P less than 0.005) pressures were significantly higher after the low-potassium diet than after the normal-potassium diet. Potassium depletion suppressed plasma aldosterone levels but had no effect on plasma renin activity or on arginine vasopressin or catecholamine levels. A saline infusion further increased the mean arterial pressure in the potassium-depleted subjects but had no effect in the control group (P less than 0.05). We conclude that short-term potassium depletion increases blood pressure in healthy, normotensive men and permits further increases in blood pressure after saline loading. We found no evidence that the hypertensive effect of potassium depletion resulted from changes in either renal hemodynamics or circulating levels of vasoactive hormones.
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PMID:Increased blood pressure during potassium depletion in normotensive men. 281 51

The purpose of this study was to investigate the renal handling of sodium and potassium in rats during an acute ethanol (ETOH) administration and to relate any observed changes to alterations in renin-aldosterone secretion. Eight male Wistar rats, 7 to 8 weeks of age, were injected intraperitoneally (IP) with 1.0 g/kg body wt. ETOH (15% v/v, 95% ETOH in saline, pH 6.98, osmolality 284 mOsm/kg). Blood ETOH levels were 159 +/- 16 (Mean +/- SEM) and 120 +/- 12 mg/dl, 10 and 30 min after the ETOH injection respectively (p less than 0.05). Control animals were given either an equal volume (1.77 ml/100 g body wt.) of 0.9% saline (n = 6) or 5% dextrose solution (n = 4) with similar pH and osmolality. Following ETOH administration blood pH, urine pH, plasma bicarbonate (HCO3) concentration declined significantly (p less than 0.01) while glomerular filtration rate (GFR) and hematocrit (Hct) remained unchanged (p = 0.1). Mean fractional sodium excretion (FENa), fractional potassium excretion (FEK), and osmolar clearance (Cosm) fell significantly despite an increase in plasma sodium (p less than 0.01), potassium (p less than 0.05) and osmolality concentrations (p less than 0.05). There was no significant change in plasma aldosterone concentration (PA) or plasma renin activity (PRA) following the ETOH administration. No difference in GFR, FENa, FEK, Cosm, blood pH, urine pH, plasma electrolytes, PA, or PRA was observed following the saline or dextrose injections. In conclusion, acute ETOH administration in rats alters renal sodium and potassium excretion independent of changes in GFR, PA, PRA or plasma volume as reflected by Hct.
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PMID:Acute effect of ethanol on renal electrolyte excretion in rats. 266 Aug 49

Sodium, phosphorus, chloride and potassium concentrations were measured by a new method in individual principal and intercalated cells in the cortical collecting duct in vitro. Electron microprobe analysis was applied to freeze-dried cryosections of the isolated perfused rabbit cortical collecting duct. Cell analyses were performed under control conditions and after addition of ouabain to the bath. Under control conditions similar sodium, potassium, chloride, and phosphorus concentration (means +/- SEM) were observed in principal (10.0 +/- 0.6, 126.5 +/- 2.7, 24.6 +/- 1.0, and 121.5 +/- 3.5 mmol/kg wet weight, respectively) and intercalated cells (9.0 +/- 0.9, 127.1 +/- 4.2, 27.4 +/- 1.8, and 118.7 +/- 4.9 mmol/kg wet weight, respectively). In principal cells ouabain (10 min) caused an increase in sodium and chloride concentrations by 104 and 13 mmol/kg wet weight, and a decrease in potassium and phosphorus concentrations by 106 and 32 mmol/kg wet weight. These changes in cell element concentrations can be ascribed to an exchange of intracellular potassium against extracellular sodium and to cell swelling due to influx of extracellular fluid. The effects of ouabain on intercalated cells were far less pronounced than on principal cells. This different susceptibility to ouabain of principal and intercalated cells can be ascribed to differences in active and passive transmembrane ion transport pathways.
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PMID:Effect of ouabain on electrolyte concentrations in principal and intercalated cells of the isolated perfused cortical collecting duct. 272 28

Bartter's syndrome is characterized by chronic hypokalaemia, activation of the renin-angiotensin system and normal blood pressure. To investigate whether a generalized disturbance of sodium-potassium pump function might be of pathogenetic importance, lymphocytic sodium-potassium homeostasis was examined in 5 patients suffering from Bartter's syndrome. Two of the patients were treated with potassium chloride supplementation, the others were without medical treatment when studied. All were severely hypokalemic (serum potassium 2.8 +/- 0.24 mmol/l, mean +/- SEM). Lymphocyte sodium and potassium concentration (14.4 +/- 0.37 and 94.4 +/- 7.7 mmol/l, respectively), ouabain sensitive 22Na-efflux rate constant (2.68 +/- 0.25 h), and absolute ouabain sensitive efflux rate (38.16 +/- 4.2 mmol l-1 h) did not differ from matched controls. Ouabain binding capacity was 126 900 +/- 23 500 sites/cell in patients vs 50 400 +/- 17 900 in controls (p less than 0.05). In conclusion, patients with Bartter's syndrome may have an intrinsic abnormal pump function, characterized by an increased pump density and a low cation turn-over rate per pump unit.
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PMID:Lymphocytic sodium and potassium pump function in Bartter's syndrome. 274 41


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