Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: KEGG:D05329 (Ringer's solution)
2,826 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was initiated with the hope of clarifying the role of negative charges in the luminal brush border membrane in the overall process of trans-epithelial isotonic sodium and water absorption. Using micropuncture techniques, cationic polyamino acids such as polylysine (mol wt 100,000, 17,000 and 1,500-5,000, 1 mg/ml), tetralysine, polyornithine (mol wt 100,000, 1mg/ml), polyethyleneimine (2 mg/ml), polymyxin B (2 mg/ml), protamine sulfate (25 mg/ml) and histone (0.5 mg/ml) were perfused through the segments of rat kidney proximal tubule for 30 sec to 2 min. The rate of isotonic fluid absorption was measured before and after each perfusion with the Gertz's split drop method using Ringer's solution as a shrinking drop. Polylysine 100,000 and 17,000 and polyornithine were the most potent, inhibiting isotonic reabsorption by 93%. The sequence of inhibitory effect was: polylysine 100,000 congruent to polyornithine 100,000 congruent to polylysine 17,000 greater than polyethyleneimine greater than polylysine 1,500-5,000 congruent to polymyxin B greater than protamine sulfate congruent to histone. In contrast, tetralysine (2 mg/ml) showed no inhibitory effect. Electrical potential difference (p.d.) of the proximal tubular cells was destroyed within 10 sec of luminal perfusion with polylysine 100,000 (1 mg/ml). Simultaneously with the drop in p.d., electrical resistance of the luminal brush border membrane was nearly totally eliminated, whereas transepithelial input resistance remained unaltered. Furthermore, trypan blue dye was taken up by polylysine 100,000-perfused tubular cells but not by normal cells. Expanding drop analysis (mannitol solution as a split drop) was performed as a screening test to examine if the permeability for water and sodium in the lateral paracellular pathway is altered by polylysine 100,000. No significant difference was observed in the velocity of split drop expansion between untreated and polylysine-perfused tubules. A lower concentration of polylysine 100,000 (0.1 mg/ml) showed a much less inhibitory effect on fluid absorption and on cell p.d. These observations indicate that the strong inhibition on proximal tubular fluid absorption exerted by polylysine and perhaps also by other cationic polyamino acids is due not to modification of membrane negative charges but to the lysis of tubular cells by these polycations.
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PMID:Mechanism of inhibition of the proximal tubular isotonic fluid absorption by polylysine and other cationic polyamino acids. 17 34

This free-flow micropuncture study examined the dependence of bicarbonate reabsorption in the rat superficial proximal convoluted tubule to changes in filtered bicarbonate load, and thereby the contribution of the proximal tubule to the whole kidney's response to such changes. The independent effects of extracellular fluid (ECF) volume expansion and of acidosis on proximal bicarbonate reabsorption were also examined. When the plasma volume contraction incurred by the micropuncture preparatory surgery was corrected by isoncotic plasma infusion ( congruent with1.3% body wt), single nephron glomerular filtration rate (SNGFR), and the filtered total CO(2) load increased by 50%. Absolute proximal reabsorption of total CO(2) (measured by microcalorimetry) increased by 30%, from 808+/-47 during volume contraction to 1,081+/-57 pmol/min.g kidney wt after plasma repletion, as fractional total CO(2) reabsorption decreased from 0.90 to 0.77. Aortic constriction in these plasma-repleted rats returned the filtered load and reabsorption of total CO(2) to the previous volume contracted levels. In other animals isohydric ECF expansion with plasma (5% body wt) or Ringer's solution (10% body wt), or both, produced no further diminution in fractional proximal total CO(2) reabsorption (0.76-0.81). Metabolic acidosis was associated with very high fractional proximal total CO(2) reabsorptive rates of 0.82 to 0.91 over a wide range of SNGFR and ECF volumes. At a single level of SNGFR, end-proximal total CO(2) concentration progressively decreased from 5.6+/-0.5 to 1.6 +/-0.2 mM as arterial pH fell from 7.4 to 7.1. Expansion of ECF volume in the acidotic rats did not inhibit the ability of the proximal tubule to lower end-proximal total CO(2) concentrations to minimal levels. In conclusion, bicarbonate reabsorption in the superficial proximal convoluted tubule is highly load-dependent (75-90%) in normal and acidotic rats. No inhibitory effect of ECF volume per se on proximal bicarbonate reabsorption, independent of altering the filtered bicarbonate load, could be discerned. Acidosis enabled the end-proximal luminal bicarbonate concentration to fall below normal values and reduced distal bicarbonate delivery.
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PMID:Control of proximal bicarbonate reabsorption in normal and acidotic rats. 50 Aug 4

Transepithelial potential difference (p.d.) was measured in the proximal tubule of Necturus kidney in vivo, by means of microelectrodes filled either with a 3M KClion or with a Ringer's solution for amphibians. The average transepithelial p.d., measured with KCl-tips, was: -1.4 +/- 2.4 mV (early convolutions), -0.1 +/- 2.0 mV (middle convolutions) and +0.1 +/- 2.4 mV (straight segment). The corresponding values obtained with Ringer's-filled microelectrodes were -2.3 +/- 1.8 mV, -1.3 +/- 1.1 mV and +0.1 +/- 1.2 mV, respectively. Tip localization into the lumen was ascertained by luminal injection of either oil (KCl electrode measurements) or artificial solutions which produced a measurable shift of transepithelial p.d. (determinations obtained with Ringer's-tips). Transepithelial p.d. in split-drops (mean reabsorptive half time 27.1 +/- 2.5 min) was -1.8 +/- 1.1 mV. The magnitude of transepithelial p.d. is discussed with respect to an equivalent electrical circuit; it is shown that high transepithelial p.d.'s are inconsistent with the known values of relative conductances of cell membranes in series and shunt pathway, respectively.
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PMID:Transepithelial potential difference in the proximal tubule of necturus kidney. 94 43

The effect of increased peritubule capillary oncotic pressure on sodium reabsorption by the proximal tubule of the dog was investistigated after extracellular volume expansion (ECVE) with Ringer's solution or during continued hydropenia. Control measurements were made after ECVE or during hydropenia and again during renal arterial infusion with hyperoncotic albumin solution. Absolute reabsorption by the proximal tubule was calculated from fractional reabsorption and single nephron filtration rates as determined by micropuncture. Direct measurements of efferent arteriole protein were used to determine efferent arteriolar oncotic pressure. Albumin infused into the renal artery after ECVE significantly increased efferent oncotic pressure by 17.6 plus or minus 5.3 mm Hg. Fractional and absolute reabsorption by the proximal tubule increased from 20 plus or minus 6 to 37 plus or minus 5% and from 22 plus or minus 6 to 36 plus or minus 7 nl/min, respectively. During hydropenia, the albumin infusion significantly increased efferent oncotic pressure by 15.0 plus or minus 4.4 mm Hg. However, in contrast to the effect seen during ECVE, neither fractional nor absolute reabsorption was changed, delta equals 0.3 plus or minus 1.5% and 3 plus or minus 5 nl/min, respectively. Single nephron filtration rates were not significantly different between the groups and were unchanged by the albumin infusion. Peritubule capillary hydrostatic pressures, measured with a null-servo device, were not changed by the albumin infusion in either group. Renal interstitial hydrostatic pressure, measured from chronically implanted polyethylene capsules, was decreased significantly from 7.2 plus or minus 0.9 to 3.4 plus or minus 0.6 mm Hg in the hydropenic group and from 0.6 plus or minus 0.6 to 4.8 plus or minus 0.7 mm Hg in the Ringer's expanded group. In the hydropenic group, the increase in efferent oncotic pressure was nearly compensated for by changes in interstitial forces so that the calculated net force for capillary uptake was almost unchanged, 17.8 mm Hg before vs. 21.4 mm Hg during the albumin infusion. The increased efferent oncotic pressure in the Ringer's expanded group was not compensated, so that the calculated net force for uptake was increased, 11.9 mm Hg before to 22.2 mm Hg during the albumin infusion. Thus, while the increase in efferent oncotic pressure during albumin infusion was not significantly different between the groups, absolute and fractional reabsorptions were increased only in the animals in which the extracellular volume was expanded. The results suggest that ECVE alters the effect of increased peritubule oncotic pressure on sodium reabsorption by the proximal tubule.
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PMID:Effect of increased peritubule protein concentration on proximal tubule reabsorption in the presence and absence of extracellular volume expansion. 111 68

The effect of foreign anions on transepithelial potential difference and transepithelial input conductance was studied in the isolated perfused Necturus kidney. Two microelectrodes (recording and current-injecting) were inserted into the lumen of single proximal tubules and the peritubular perfusate was shifted reversibly for 30-60 sec from a physiologic Ringer's solution to a test solution in which chloride was replaced isosmotically by a foreign anion. The permeability sequence, obtained by potential measurements, was: lactate less than glutamate less than gluconate less than pyruvate less than benzene sulfonate less than or equal to acetate less than or equal to F less than propionate less than BrO3 less than formate less than ClO3 less than Cl than ClO4 less than I less than or equal to Br less than NO3 less than SCN. Transepithelial conductance decreased when the tissue was perfused with anions less permeable than chloride but the conductance sequence was different from the permeability sequence. Such discrepancies were more pronounced during perfusion with hyperpolarizing anions; ClO4 and I- (both more permeable than chloride) produced an important decrease in transepithelial conductance, followed by incomplete reversibility when the perfusion was shifted again to chloride Ringer's. The results are best explained by the presence of weak positive fixed charges, governing anion permeation, at the shunt pathway of the proximal tubule. An analysis of the data allows tentative estimates of shape and size of the sites.
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PMID:Anion permeation in the proximal tubule of Necturus kidney: the shunt pathway. 121 81

Active transport potentials were studied across early loops of rat proximal tubule during luminal perfusion and peritubular superfusion with HCO3- Ringer's solution of identical ionic composition. From the effects of the carbonic anhydrase inhibitor acetazolamide and of ouabain it is concluded 1. that the lumen-positive active transport potential indicates an excess of active H+ secretion/HCO3- absorption over active Na+ absorption and 2. that the lumen-negative active transport potential, which develops in the presence of glucose (and/or aminoacids) in the tubular lumen, indicates stimulation of active Na+ absorption. Ouabain did not abolish the lumen-positive potential difference suggesting that active H+/HCO3- transport and active Na+ transport may be to some extent independent. Among the diuretics tested the mercurial diuretic mersalyl acted primarily on Na+ transport, and furosemide acted on HCO3- transport, whereas the effect of ethacrynic acid appeared to be unspecific.
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PMID:Effect of inhibitors and diuretics on electrical potential differences in rat kidney proximal tubule. 123 86

Our previous studies have shown that a low dose of angiotensin II (Ang II) stimulates fluid and bicarbonate absorption from the apical side of rat proximal tubule (PCT). These effects can be blocked by Ang II antagonist, (Sar1, Ile8)Ang II. The cellular mechanism underlying Ang II action, however, remained unclear. Thus, this study was designed to investigate the possible role of phosphoinositide turnover in mediating this action of angiotensin. Rat PCT was perfused in vivo with Ringer's solution containing [3H]inulin as a volume marker. Bicarbonate flux (JHCO3) was determined by total CO2 changes between the collected fluid and the original perfusate as analyzed by microcalorimetry. Luminal perfusion of 10(-11) M Ang II stimulated both JHCO3 and fluid reabsorption. These effects could be blocked by 10(-3) M amiloride and 10(-5) M ethylisopropylamiloride. Luminal perfusion of 4 beta-phorbol-12-myristate-13-acetate (10(-8) M) also stimulated both fluid reabsorption and JHCO3. These effects could also be blocked by amiloride and ethylisopropylamiloride. When both Ang II (10(-11) M) and 4 beta-phorbol-12-myristate-13-acetate (10(-8) M) were perfused together, the stimulatory effects on fluid reabsorption and JHCO3 were not additive. These results suggest that Ang II interacts with its receptors on the apical membrane leading to modulation of the Na-H exchange mechanism in PCT. The phosphoinositide turnover may play an important role in the Ang II action on PCT transport.
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PMID:Mechanism of angiotensin II action on proximal tubular transport. 231 94

The initial mechanisms of injury to the proximal tubule following exposure to nephrotoxic heavy metals are not well established. We studied the immediate effects of silver (Ag+) on K+ transport and respiration with extracellular K+ and O2 electrodes in suspensions of renal cortical tubules. Addition of silver nitrate (AgNO3) to tubules suspended in bicarbonate Ringer's solution caused a rapid, dose-dependent net K+ efflux (Km = 10(-4) M, Vmax = 379 nmol K+/min/mg protein) which was not inhibited by furosemide, barium chloride, quinine, tetraethylammonium, or tolbutamide. An increase in the ouabain-sensitive oxygen consumption rate (QO2) (13.9 +/- 1.1 to 25.7 +/- 4.4 nmol O2/min/mg, P less than 0.001), was observed 19 sec after the K+ efflux induced by AgNO3 (10(-4) M), suggesting a delayed increase in Na+ entry into the cell. Ouabain-insensitive QO2, nystatin-stimulated QO2, and CCCP-uncoupled QO2 were not significantly affected, indicating preserved function of the Na+,K+-ATPase and mitochondria. External addition of the thiol reagents dithiothreitol (1 mM) and reduced glutathione (1 mM) prevented and/or immediately reversed the effects on K+ transport and QO2. We conclude that Ag+ causes early changes in the permeability of the cell membrane to K+ and then to Na+ at concentrations that do not limit Na+,K+-ATPase activity or mitochondrial function. These alterations are likely the result of a reversible interaction of Ag+ with sulfhydryl groups of cell membrane proteins and may represent initial cytotoxic effects common to other sulfhydryl-reactive heavy metals on the proximal tubule.
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PMID:Silver ion (Ag+)-induced increases in cell membrane K+ and Na+ permeability in the renal proximal tubule: reversal by thiol reagents. 245 93

Amphotericin B, a polyene antibiotic known to induce cation-selective pore formation in biological cell membranes, was given to rats by peritoneal injection (10 mg/kg for 21-26 days) or added to luminal perfusates (2 x 10(-5) M). Kinetics of tubular acidification and alkalinization after perfusion with alkaline or acid phosphate Ringer's solution was studied by means of double barrelled antimony/reference microelectrodes in cortical distal tubules. Stationary pH increased both in early and late distal segments. Acidification and alkalinization half-times decreased markedly from 15-18 s to 6-8 s, a value similar to that found in proximal tubule. Net H-ion secretion rates as well as H-ion back-flux approximately doubled after Amphotericin B. Apparent H-ion permeability of distal tubule epithelium measured during perfusion of lumen and peritubular capillaries with phosphate Ringer's solutions doubled both in early and late segments. These data show that amphotericin B produces a distal acidification defect which impairs formation of normal transepithelial pH gradients by increasing H-ion back-flux without reducing rates of net H-ion secretion.
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PMID:Effect of amphotericin B on renal tubular acidification in the rat. 271 75

The role of the proximal tubule in the natriuresis after volume expansion was investigated by evaluating sodium excretion both in the presence and absence of increased delivery from the proximal tubule. Proximal delivery was calculated from fractional reabsorption in superficial proximal tubules determined by micropuncture and glomerular filtration rate of the micropunctured kidney. Infusion of Ringer's solution in six dogs increased delivery from the proximal tubule 4.7+/-1 ml/min (P < 0.01) and increased fractional sodium excretion 3.6+/-1.1% (P < 0.025). Infusion of hyperoncotic albumin into the renal artery during sustained volume expansion decreased delivery from the proximal tubule 6.5+/-0.9 ml/min (P < 0.01). Although proximal delivery was restored to below control levels, fractional sodium excretion was significantly increased 2.5+/-0.5% (P < 0.01) as compared with the hydropenic control period. Fractional phosphate excretion was increased 15.5+/-3.7% (P < 0.01) after Ringer's infusion and was decreased 10.5+/-1.6% (P < 0.005) after intrarenal albumin infusion, suggesting that changes in superficial nephron reabsorption were paralleled by changes in reabsorption in deeper nephrons. Similar results were found in six additional dogs in which other factors known to affect phosphate reabsorption were controlled; however, these studies cannot completely eliminate a role for deep nephrons in the natriuresis after intrarenal albumin infusion. Since 70% of the natriuresis after volume expansion was present without increased delivery from superficial proximal tubules, it is likely that increased delivery from the proximal tubule contributes a relatively minor fraction to the natriuresis of volume expansion.
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PMID:Effect of volume expansion on sodium excretion in the presence and absence of increased delivery from superficial proximal tubules. 471 57


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