UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the cellular mechanism of urinary acidification in detail, micropuncture studies were performed on the in situ bullfrog proximal tubule with nigericin-based pH microelectrodes. Pencil-type double-barreled antimony microelectrodes were also used for monitoring pHs of the tubular fluids. Luminal perfusion of 10(-3) M cyanide caused a biphasic change in cell pH (pHi): i.e., early acidification by 0.04 pH unit in 2 min and later alkalinization by 0.04. A profound depolarization of 30-35 mV was observed in the peritubular membrane potential (EM Peri), although the tubular fluid pH (pHTF) was elevated by 0.11 unit. Luminal substitution of 100 mM Na+ by Li+ acidified the cell by 0.06 pH unit with a depolarization of EM Peri by 8 mV and an alkalinization of pHTF by 0.10 unit. It is a fact that cellular acidification and luminal alkalinization are in good agreement with the depression of luminal H+ secretory mechanism. Perfusion of 10(-4) M SITS from the peritubular side caused a rise in pHi by 0.04 without appreciable changes in EM Peri in the short period application. Peritubular perfusion of 10(-4) M ouabain lowered the pHi by 0.07 with a resulting depolarization of EM Peri by 15.4 mV, meanwhile, the pHTF, while initially lowered by 0.07 unit, was elevated 4 min later by 0.12. Inhibitions of the peritubular ion transport mechanism caused some pH changes in the same direction, both in the cell interior and the tubular fluid. Further, from the ouabain experiment, it is inferred that some linkages, mediated by Na+ and H+(or HCO3-), would exist between the peritubular and luminal membranes.
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PMID:Regulatory mechanism of cell pH in the renal proximal tubule of bullfrog nephron. 300 93

Young male mice were given drinking water containing 50 ppm cadmium (Cd) for 3 weeks, and were killed 0, 3 and 6 weeks after the cessation of treatment. At 0 weeks, suppression in the number of splenic plaque-forming cells in response to sheep red blood cell immunization was noted 5 days after antigen injection, but not 7 days after injection. Plasma IgG concentration and thymic factor activity were unaffected at 0 weeks. The number of circulating lymphocytes tended to be less in the Cd-treated mice at all times. Cd treatment had no effect upon liver and kidney weights, and upon the weights and the lymphocyte contents of the thymus and spleen at any of the observation times. Employing immunofluorescence with anti-mouse IgG and C3, no evidence of an autoimmune response was found in the kidney of the treated mice at 0 and 3 weeks. Mitochondrial abnormalities in the renal proximal tubule cells were noted at 0 weeks in the Cd-treated mice. The Cd concentrations of the liver and kidneys remained high at all observation times. The results suggest that a modest dose of Cd produces some depression of the immune system, and the biological half-life of Cd is long.
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PMID:Immunopathology of chronic cadmium administration in mice. 353 68

The long-term effects of cyclosporine on renal function were evaluated in eleven liver transplant recipients over a 6-26-month follow-up period. Renal hemodynamic function (glomerular filtration rate [GFR], effective renal plasma flow [ERPF]) fell 60% postoperatively, subsequently improved, and stabilized at 45-60% of normal despite continued drug administration. Tubular sodium transport studies during water diuresis suggested that the proximal tubule is a major site of cyclosporine nephrotoxicity. In contrast to the acute effects of cyclosporine on renal function, the fraction of glomerular filtrate reabsorbed in the proximal tubule was less in the patient group while the fractional excretion of sodium, potassium, and phosphate was increased. When the fraction of filtered sodium reabsorbed in the diluting segment was examined as a function of sodium delivery, functional impairment occurred in the diluting segment as well. Eight renal biopsies performed in six patients 4-29 months posttransplantation showed only mild to moderate changes, predominantly vascular, which correlated poorly with corresponding renal function. These data showed that long-term cyclosporine administration produced early and persistent depression of both hemodynamic and tubular function. A functional rather than structural mechanism appears to be more significant during this period of observation.
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PMID:Long-term effects of cyclosporine on renal function in liver transplant recipients. 355 55

Organic ion transport across the basolateral membrane of proximal tubules was measured by means of the tissue slice technique in each of the four different stages of Heymann nephritis. Impairment of both organic anion and cation transport was detected early in Stage 2, and became more severe in Stage 3 of Heymann nephritis. The decreased transport function was associated with extensive damage to proximal tubule cells, including loss of brush border microvilli and basal infoldings. Despite these abnormalities of structure and function, oxygen consumption of proximal tubule cells remained essentially normal. Partial recovery of organic cation transport was noted late in Heymann nephritis (Stage 4). Recovery of the cation transport function was associated with a partial restoration of brush border microvilli and basal infoldings to proximal tubule cells. However, organic anion transport remained depressed throughout the entire course of disease. Impairment of organic ion transport in rats with Heymann nephritis appeared to result from damage to basolateral membrane transport elements rather than general deterioration of the metabolic machinery of proximal tubule cells. Decreased organic cation transport appeared to be the consequence of a reduction in the number of carrier sites, a phenomenon that could have resulted from decreased membrane surface area. However, the depression of organic anion transport was associated with decreased substrate affinity of the anion carrier, indicating that qualitative, rather than quantitative changes, were primarily responsible for that defect. Specific antibody-mediated damage to the anion transport elements in basolateral membranes of proximal tubules is postulated to occur in Heymann nephritis.
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PMID:Impaired organic ion transport in proximal tubules of rats with Heymann nephritis. 387 61

The effect of phosphate infusion on renal tubular handling of calcium and phosphate was examined in dogs which had been thyroparathyroidectomized (TPTX) immediately prior to the studies. Phosphate infusions in TPTX animals caused a small decrease in total and ultrafilterable plasma calcium, and decreased phosphate reabsorptive capacity in the proximal tubule and loop segment. Infusion of CaCl2 during phosphate loading to offset the fall in plasma calcium prevented the reduction in proximal phosphate reabsorptive capacity. However, between the proximal and distal sampling site, the reduction in phosphate reabsorptive capacity could not be prevented by CaCl2 administration. These data are consistent with the presence of two phosphate transport systems; one in the early proximal tubule, modulated by changes in plasma calcium level, and a second in the loop segment, which is independent of calcium. While the data suggest that the depression of proximal phosphate reabsorption during phosphate infusion may be secondary to the fall in plasma calcium concentration, they do not exclude a direct effect of infused phosphate on proximal phosphate reabsorption that may be antagonized by an opposing direct effect of the calcium infusion.
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PMID:Effects of phosphate and calcium infusion on renal phosphate transport in the dog. 396 6

The absolute rate of reabsorption by superficial rat proximal tubules was measured by the in situ microperfusion technique under conditions of hydropenia, infusion of saline, and infusion of saline plus aortic constriction sufficient to decrease whole kidney filtration rate below hydropenic levels. Fractional reabsorption was measured in adjacent filtering nephrons by collecting and recollecting tubular fluid from late proximal convolutions during each experimental condition. During hydropenia, the absolute rate of proximal tubular reabsorption averaged 3.56 +/-0.60 nl/min per mm and late proximal tubular fractional reabsorption averaged 0.56 +/-0.10. From these two measurements and measurements of tubule length to the site of micropuncture, a value for filtration rate was calculated for filtering nephrons. During hydropenia this value averaged 32.9 +/-7.1 nl/min. Saline infusion increased sodium excretion to 5.5% of the filtered load as the absolute rate of proximal tubular reabsorption decreased 38% and fractional reabsorption decreased 45%. Calculated superficial nephron filtration rate increased 21% which on the average was identical with the simultaneously measured increase in whole kidney filtration rate. Similar results were obtained in a separate group of animals by the technique of total collection of late proximal tubular fluid. Aortic constriction during saline infusion decreased whole kidney and calculated nephron filtration rate to the same degree and to values lower than those during hydropenia. Fractional reabsorption increased but not to hydropenic values. The persistent natriuresis during aortic constriction was associated with a continued depression of the absolute rate of proximal tubular reabsorption which was sufficient to maintain an increased delivery of filtrate out of the proximal tubule despite the fall in nephron filtration rate. These results indicate that depressed fractional reabsorption in the proximal tubule during acute saline infusion is due predominantly to a decrease in absolute reabsorptive rate and to a lesser extent to an increase in superficial nephron filtration rate which is proportional to the increase in whole kidney filtration. Continued natriuresis when filtration rate is decreased during saline infusion can be accounted for entirely by the persistent large reduction in the absolute rate of proximal tubular reabsorption.
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PMID:The relative contributions of reabsorptive rate and redistributed nephron filtration rate to changes in proximal tubular fractional reabsorption during acute saline infusion and aortic constriction in the rat. 511 9

The evidence from previous micropuncture studies for an inhibitory effect of furosemide on proximal sodium reabsorption in the rat has been conflicting. Intrinsic reabsorptive capacity, estimated in free flow and shrinking drop experiments, has been reported to be depressed, whereas fractional reabsorption usually remains unchanged. We have recently reported that, during conditions of elevated intraluminal hydrostatic pressure, unless care is taken to prevent retrograde flow of tubule fluid from more distal sites, the concentration of inulin in late proximal fluid is often factitiously elevated. Since furosemide raises intraluminal pressures, often markedly, the failure to detect a depression of fractional reabsorption might be the consequence of retrograde contamination during fluid collection. Experiments were designed to compare the effect of furosemide on fractional sodium reabsorption by the proximal tubule when collections were obtained with distal oil blocks of conventional length as well as with unusually long blocks of oil of low and high viscosities. When reflux is prevented, fractional sodium reabsorption is usually depressed by furosemide, whereas when conventional distal blocks are used, the calculated values for fractional reabsorption either remain unchanged or increase. Simultaneous measurements of nephron glomerular filtration rate indicate that the latter is the consequence of retrograde contamination.
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PMID:An inhibitory effect of furosemide on sodium reabsorption by the proximal tubule of the rat nephron. 576 11

The concept that acute increases in glomerular filtration rate (GFR) will cause large concomitant increases in sodium excretion has been re-examined. In previous work, GFR was elevated by volume expansion, usually with saline infusions. Recent evidence shows that tubular reabsorption is depressed during saline loading; hence, the independent effect of increased GFR on sodium excretion cannot be assessed.TO DETERMINE THE EFFECT OF ACUTE INCREASES IN GFR PER SE ON SODIUM EXCRETION, WE RAISED GFR BY FOUR TECHNIQUES NOT INVOLVING VOLUME EXPANSION: protein feeding, dopamine infusion, intravenous dexamethasone, and cross-circulation. GFR increased acutely by 5 to 85% in these experiments. In 12 of 24 experiments, GFR increased by more than 30%. In all but one experiment, sodium excretion increased by less than 75 muEq per minute. Data from experiments using each of the four techniques were comparable. The results were the same whether mineralocorticoid activity was high or low. In contrast, during saline loading, sodium excretion increased more than 800 muEq per minute with equal or lesser changes in GFR. These results demonstrate that acute increases in GFR per se have little effect on sodium excretion. We suggest that, due to constant fractional sodium reabsorption in the proximal tubule (glomerulotubular balance) and increased distal reabsorption, virtually all of the increase in filtered sodium is reabsorbed when GFR increases. Depression of tubular reabsorption is required for natriuresis.
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PMID:Evidence that an acute increase in glomerular filtration has little effect on sodium excretion in the dog unless extracellular volume is expanded. 601 63

The purpose of this investigation was: (1) to establish a simplified radioimmunoassay (RIA) for quantitating renal tubular epithelial antigens (RTE) in urine; (2) to ascertain whether urine RTE concentrations as measured by this technique correlate with the severity of acute nephrotoxic and ischemic injury; and (3) to ascertain whether increased urinary RTE is a specific marker of renal tubular injury. A direct binding RTE RIA was established using 125I labelled anti-RTE antibody and 10% polyethylene glycol to separate bound from unbound anti-RTE 125I. This RIA is simpler than previously described RTE assay methods since: (1) double antibody separation techniques are eliminated; (2) RTE antigen purification from crude proximal tubular fragments is no longer necessary; and (3) immunoglobulin G(IgG) rather than more radiosensitive RTE is used as the radioligand. To test the utility of this assay as a marker of acute tubular injury anesthetized rats were subjected to graded nephrotoxic (HgCl2: 0--20 mg/kg) or bilateral renal ischemic (0--32 min) insults. Glomerular filtration rates (GFR) (clearance iothalamate 125I) and RTE concentrations were measured sequentially. Post-renal injury, RTE concentrations rose above control values and the degree of elevation strongly correlated with the severity of GFR depression (r = 0.72--0.81; p less than 0.02--0.05). The source of this increased urinary RTE was the proximal tubule since brush border loss was demonstrated histologically and because no RTE could be detected in serum. Rats whose GFRs were acutely depressed by inducing either volume depletion or acute experimental glomerulonephritis (nephrotoxic serum nephritis) all had normal urine RTE concentrations. These results suggest that RTE quantitation by this technique may provide a specific and early quantitative index of the severity of acute nephrotoxic and ischemic renal injury.
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PMID:Quantitating the severity of proximal tubular brush border injury by a simple direct binding radioimmunoassay. 621 75

Dahl described a strain of rats with genetically controlled propensities for hypertension. Chronic excess salt feeding increased blood pressure in sensitive (s) rats, whereas resistant rats (R) remain normotensive. We tested the pressure natriuretic function (urinary sodium excretion versus perfusion pressure) in isolated kidneys perfused with a cellular medium: in sodium-restricted normotensive sensitive (S0) and resistant (R0) animals; in sensitive rats receiving a high-salt diet for 3 weeks (S3): and in both S and R animals exposed to excess sodium for 7 weeks (R7 and S7). The aim of these studies was to determine if a preset alteration of the pressure natriuretic function might be present in S animals prior to the development of hypertension. Systolic blood pressure in S0, S3, and S7 animals were 123 +/- 4, 136 +/- 2, and 162 +/- 4 mm Hg, respectively, whereas that of R0 and R7 were 121 +/- 5 and 126 +/- 5 mm Hg. An increase of the perfusion pressure of isolated kidneys from 105 to 185 mm Hg in stepwise fashion resulted in a pressure natriuresis whose slope was similar in R0 and S0 animals. Of interest was that the pressure natriuretic function slope of kidneys from R0 (low sodium) and R7 (high sodium) rats was as predicted by the Guyton system analysis of normal blood pressure control Micropuncture of the proximal nephrons demonstrated that the origin of the natriuresis resulted from a site beyond the accessible proximal tubule. Results from S7 kidneys contrasted with all others in that the natriuretic response was depressed (P less than 0.01), which resulted from significantly lower filtration rates at higher perfusion pressures. We concluded (1) in normal R rats, the pressure natriuretic function is that predicted by the Guyton hypothesis, (2) Dahl S animals have no preset abnormality of this function until hypertension is present for some time, and (3) a depression of the pressure natriuretic function may aggravate hypertension in S rats once high blood pressure has persisted.
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PMID:Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats). 721 56

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