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G Malnic

Publications and source records attributed to G Malnic.

At least 37 records · Page 2Linked to original sources
PubMed1996

Regulation of rat proximal tubule Na/H exchange by protein kinase C.

The effect of protein kinase C (PKC) activation on fluid and bicarbonate transport in renal tubules has been discussed controversially. Stimulation and inhibition have been shown to depend on factors such as experimental model and exposure time to the mediator of enzyme activation. We studied the role of PKC activation by phorbol-12-myristate-13-acetate (PMA) and by 1,2-dioctanoyl glycerol (DOG) in proximal bicarbonate reabsorption (JHCO3-) by 'in vivo' stationary microperfusion and ion-exchange resin microelectrode determination of luminal pH. Both PMA (10(-8) mol/l) and DOG (10(-3) mol/l) added to lumen or to peritubular capillaries reduced the net JHCO3- significantly. When added to lumen, the inhibition was 44 and 32%, respectively. This reduction did not involve changes in lumen stationary pH, but was mediated by a marked increase in the halftime of luminal bicarbonate disappearance; from 4.22 +/- 0.23 to 6.27 +/- 0.51 s with PMA and from 3.90 +/- 0.25 to 6.33 +/- 0.48 s with DOG. This effect was intensified by 10(-6) mol/l okadaic acid, a phosphatase inhibitor (inhibition of JHCO3- increased to 61%), and reduced by 30% by 10(-6) mol/l H7, an inhibitor of PKC. H89, a protein kinase A inhibitor, did not affect the inhibitory action of PMA. Our data suggest that PKC activation reduces the rate of H ion secretion (bicarbonate reabsorption) in convoluted segments of rat renal proximal tubules and that phosphorylation of the Na+/H+ exchanger by this kinase is the cause of the reduction in net secretion of H ions.

Acids↗
PubMed1995

Secretion of HCO3-/OH- in cortical distal tubule of the rat.

Secretion of bicarbonate has been described for distal nephron epithelium and attributed to apical Cl-/HCO3- exchange in beta-intercalated cells. We investigated the presence of this mechanism in cortical distal tubules by perfusing these segments with acid (pH 6) 10 mM phosphate Ringer. The kinetics of luminal alkalinization was studied in stationary microperfusion experiments by double-barreled pH (ion-exchange resin)/1 M KCl reference microelectrodes. Luminal alkalinization may be due to influx (into the lumen) of HCO3- or OH-, or efflux of H+. The magnitude of the Cl-/HCO3- exchange component was measured by perfusing the lumen with solutions with or without chloride, which was substituted by gluconate. This component was not different from zero in control and alkalotic (chronic plus acute) Wistar rats. Homozygous Brattleboro rats (BRB), genetically devoid of antidiuretic hormone, were used since this hormone has been shown to stimulate H+ secretion, which could mask bicarbonate secretion. In these rats, no evidence for Cl-/HCO3- exchange was found in control BRB and in early distal segments of alkalotic animals, but in late distal tubule a significant component of 0.14 +/- 0.033 nmol/cm2.sec was observed, which, however, is small when compared to the reabsorptive flow found in control Wistar rats, of 0.95 +/- 0.10 nmol/cm2.sec. In addition, 5 x 10(-4) M SITS had no effect on distal bicarbonate reabsorption in controls as well as on secretion in alkalotic Wistar and Brattleboro rats, which is compatible with the absence of effect of this drug on the apical Cl-/HCO3- exchange in other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1994

Mechanism of acidification along cortical distal tubule of the rat.

The cellular mechanism of luminal acidification (bicarbonate reabsorption) was studied in cortical distal tubules of rat kidney. The stopped-flow microperfusion technique was applied to early distal (ED) and late distal (LD) segments, perfused with bicarbonate Ringer solution to which specific inhibitors were added, to measure bicarbonate reabsorption [HCO3 flux (JHCO3)]. pH and transepithelial potential difference (Vt) were recorded by double-barreled H+ exchange resin/reference (1 M KCl) electrodes. Amiloride increased stationary pH and reduced Vt in both early and late segments. Hexamethylene-amiloride (HMA), a specific Na(+)-H+ exchange blocker, reduced JHCO3 in both segments (ED by 43.6 and LD by 40.3%) without affecting Vt. Benzamil, an Na(+)-channel blocker, reduced Vt by 75.9 in ED and 74.9% in LD but had no significant effect on acidification in both segments. The specific inhibitor of H(+)-ATPase, bafilomycin A1, inhibited LD JHCO3 at a concentration of 2 x 10(-7) M by 49%, but ED was inhibited by 24% only at 2 x 10(-6) M. Sch-28080, an inhibitor of gastric H(+)-K(+)-ATPase, reduced JHCO3 by 35% in LD of K(+)-depleted rats but not in control rats and had no effect on ED. These data indicate that, in ED, bicarbonate reabsorption is mediated mostly by Na(+)-H+ exchange. In LD, there is evidence for contribution of Na(+)-H+ exchange, vacuolar H(+)-ATPase, and H(+)-K(+)-ATPase (in K(+)-depleted rats) to bicarbonate reabsorption.

Amiloride↗
PubMed1994

The role of the distal nephron in the regulation of acid-base equilibrium by the kidney.

The present paper reviews mechanisms by which the kidney controls systemic acid-base balance, with emphasis on the role of the distal nephron, and particularly of the cortical distal tubule. These mechanisms are essentially based on H-ion transport along the whole nephron. In proximal tubule cells, approximately 80% of H-ion secretion is mediated by Na+/H+ exchange, and 20% by H(+)-ATPase. In the distal nephron, acid-base transport mechanisms are located mainly in intercalated cells. H-ion secretion is effected by vacuolar H(+)-ATPase in alpha-intercalated cells and, in K-depleted animals, also by the gastric type H/K ATPase. In animals in alkalosis, beta-intercalated cells secrete bicarbonate by an apical Cl-/HCO3- exchanger, while a basolateral H-ATPase transfers H-ions into the interstitium. In cortical distal tubule, these mechanisms have been shown to be present in the intercalated cells of the connecting segment and of the initial collecting duct (the late distal tubule of micropuncture experiments). In the convoluted distal tubule (early distal tubule), most H-ion secretion occurs by means of the Na+/H+ exchanger. These data show that the distal nephron, including the cortical distal tubule, is a nephron segment responsible for a sizeable portion of bicarbonate reabsorption and titratable acid generation, as well as for bicarbonate secretion under appropriate metabolic conditions, being therefore the site of fine regulation of renal mechanisms that maintain acid-base homeostasis.

Acid-Base Equilibrium↗
PubMed1993

Effect of medium tonicity on transepithelial H(+)-HCO3-fluxes in rat proximal tubule.

1. The effect of luminal and capillary perfusion with hypotonic or hypertonic solutions containing 25 mM NaHCO3 or NaH2PO4 plus NaCl, K+, Ca2+, Mg2+ and acetate at an osmolality of 100 or 500 mosmol kg-1 on rat proximal H+ secretion was estimated by monitoring luminal pH with Sb microelectrodes. The results were compared to perfusions with the same ionic concentration in which tonicity was adjusted to 300 mosmol kg-1 with raffinose. 2. The kinetics of acidification of luminally injected bicarbonate buffer permits evaluations of H(+)-HCO3-fluxes as well as stationary pH gradients; the kinetics of alkalinization of luminally injected acid phosphate buffer indicates H(+)-HCO3-backfluxes from blood to lumen. 3. In alkalinization experiments, luminal perfusion with hypotonic solution during presence of blood in capillaries or hypotonic capillary perfusion leads to a decrease of stationary pH, an increase of alkalinization half-time and consequently a decrease of passive H(+)-HCO3-backflux. 4. In alkalinization experiments, during luminal and/or capillary perfusions with hypertonic solutions, no significant differences in the stationary pH, alkalinization half-time and H(+)-HCO3-backflux were found. 5. During acidification experiments, with both hypo- and hypertonic perfusions, no significant differences in stationary pH, acidification half-time and H(+)-HCO3-flux were observed. 6. Luminal perfusion with hypotonic solution increases specific epithelial resistance in the presence of blood in capillaries. Luminal perfusion with hypertonic solution does not change this parameter. 7. Volume changes, measured by the split-drop method, are slow during the first 30 s and do not explain the increased alkalinization half-time during luminal perfusion with hypotonic solution, since this is the period of fastest pH change. 8. Luminal perfusion with hypotonic solution decreases apparent H+ permeability in the presence of blood or hypotonic solution in capillaries. Hypertonic solutions in all experimental conditions had no significant effect on this parameter. 9. The data indicate that decrease of tonicity of fluids in contact with proximal tubule epithelium affects passive H(+)-HCO3-backflux, which proceeds in part through the shunt path, while acidification (H+ secretion), which is transcellular, is not affected by extracellular tonicity.

Acid-Base Equilibrium↗
PubMed1993

Renal bicarbonate reabsorption in the rat. IV. Bicarbonate transport mechanisms in the early and late distal tubule.

Bicarbonate transport was studied in vivo by separate microperfusion experiments of early and late distal tubules. Total CO2 was measured by microcalorimetry and fluid absorption by 3H-inulin. Significant bicarbonate absorption was observed in all experimental conditions. Bicarbonate transport was load-dependent upon increasing the luminal bicarbonate concentration from 15 to 50 mM in both early and late distal tubule segments and remained constant at higher concentrations at a maximum rate of 100-110 pmol/min per mm. At low lumen bicarbonate concentrations (15 mM), higher rates of bicarbonate absorption were observed in early (32.9 +/- 4.57 pmol/min per mm) as compared to late distal tubules (10.7 +/- 3.1 pmol/min per mm). Amiloride and ethyl-isopropylamiloride both inhibited early but not late distal tubule bicarbonate absorption whereas acetazolamide blocked bicarbonate transport in both tubule segments. Fluid absorption was significantly reduced in both tubule segments by amiloride but only in early distal tubules by ethyl-isopropylamiloride. Substitution of lumen chloride by gluconate increased bicarbonate absorption in late but not in early distal tubules. Bafilomycin A1, an inhibitor of H-ATPase, inhibited late and also early distal tubule bicarbonate absorption, the latter at higher concentration. After 8 d on a low K diet, bicarbonate absorption increased significantly in both early and late distal tubules. Schering compound 28080, a potent H-K ATPase inhibitor, completely blocked this increment of bicarbonate absorption in late but not in early distal tubule. The data suggest bicarbonate absorption via Na(+)-H+ exchange and H-ATPase in early, but only by amiloride-insensitive H+ secretion (H-ATPase) in late distal tubules. The study also provides evidence for activation of K(+)-H+ exchange in late distal tubules of K depleted rats. Indirect evidence implies a component of chloride-dependent bicarbonate secretion in late distal tubules and suggests that net bicarbonate transport at this site results from bidirectional bicarbonate movement.

Acid-Base Equilibrium↗
PubMed1993

Effect of bafilomycin on proximal bicarbonate absorption in the rat.

To evaluate the relative importance of the V-type H(+)-ATPase in proximal bicarbonate reabsorption in vivo, proximal tubules of male and female Wistar rats (180 to 260 g) were perfused with bicarbonate-Ringer solution with and without the addition of 2 microM bafilomycin A1. Bafilomycin significantly increased stationary pH from 6.75 +/- 0.05 (N = 39) to 6.86 +/- 0.03 (N = 82), the stationary concentration of bicarbonate from 5.24 +/- 0.62 to 6.33 +/- 0.46 mM and the half-time of acidification from 3.72 +/- 0.22 to 4.65 +/- 0.25 s, and significantly decreased net bicarbonate reabsorption from 3.17 +/- 0.21 to 2.55 +/- 0.15 nmol s-1 cm-2, that is, by 20%. Since bafilomycin is considered to be a specific inhibitor for V-type H(+)-ATPase, these data establish 1) the existence of this type of transport in the rat proximal tubule and 2) that approximately a fifth of the total proximal bicarbonate reabsorption is due to this mechanism of transport.

Absorption↗
PubMed1993

Transepithelial pH gradients in cortical distal tubules during metabolic alkalosis.

1. The cortical distal tubule of the rat kidney participates in the regulation of acid-base balance, showing bicarbonate reabsorption, secretion or absence of transport under different experimental conditions. In the present study, we measured differences in transepithelial pH using double ion-exchange resin/reference microelectrodes in control and alkalotic (chronic plus acute) male Wistar rats and in alkalotic rats receiving a K+ supplement in diet and infusion. 2. pH was measured in the tubule lumen during stationary microperfusion with 25 mM bicarbonate Ringer solution, and in peritubular vessels next to the perfused tubules. 3. Differences in transepithelial pH were 0.70 +/- 0.12 (N = 16) pH units in early distal tubules (ED) and 1.03 +/- 0.050 (N = 15) in late distal tubules LD) of control rats, 0.22 +/- 0.056 (N = 17) in ED and 0.25 +/- 0.050 (N = 20) in LD of alkalotic rats, and -0.02 +/- 0.039 (N = 24) in ED and -0.02 +/- 0.040 (N = 24) in LD of K(+)-supplemented alkalotic rats. 4. In control rats, the transepithelial potential difference (PD) (-8.9 +/- 1.45 mV (N = 16) in ED and -32.7 +/- 2.99 mV (N = 15) in LD) was not large enough to explain transepithelial H+ and HCO3- gradients, suggesting the presence of an active transport mechanism responsible for their maintenance. 5. The present data show that the cortical distal tubule is able to establish transepithelial pH (HCO3-) differences, that these differences are reduced by alkalosis and abolished by alkalosis plus K+ supplementation, and that, although inversion of pH gradients (evidence for bicarbonate secretion) was observed in individual tubules, this inversion was not significant in the groups studied.

Acid-Base Equilibrium↗
PubMed1992

Effects of parathyroid hormone and calcium and their interrelationship on urinary acidification in the rat.

1. The influence of thyroparathyroidectomy on renal function and specifically on acid excretion was studied in rats with or without oral supplementation of calcium. 2. Thyroparathyroidectomy caused a significant decrease in glomerular filtration rate, in the urinary/plasma inulin ratio and in overall acid excretion. These changes were not corrected by calcium supplementation. 3. Rates of proximal tubular acidification were studied by means of double-barrelled resin/reference microelectrodes. Acidification half-time was significantly increased in both thyroparathyroidectomized and calcium-supplemented thyroparathyroidectomized rats (8.38 s and 7.40 s, respectively) compared with control rats (5.44 s). 4. When 10(-6) mol/l A23187, a calcium ionophore, was added to the luminal bicarbonate solution, the acidification half-time returned to 3.97 s in the thyroparathyroidectomized rats, whereas no significant changes were detected in the properties of acidification in the control rats. 5. These data show that parathyroid hormone and cellular calcium are important factors involved in proximal tubular H+ secretion, which appears to be largely dependent on a well-defined concentration range of these agents.

Animals↗
PubMed1992

Role of corticosteroids in distal acidification of amiloride-treated rats.

The role of amiloride-dependent sodium channels in the action of adrenal cortical steroids on urine-blood PCO2 (U-B PCO2) differences was studied in bicarbonate-infused and amiloride-treated adrenalectomized rats. U-B PCO2 was significantly reduced by amiloride in bicarbonate-infused control rats. Adrenalectomy further reduced U-B PCO2 in amiloride-treated, bicarbonate-infused rats (from 27.9 +/- 1.82 mmHg in sham-operated rats to 21.3 +/- 1.58 mmHg in adrenalectomized (ADX) rats) (1 mmHg = 133.322 Pa). Acute administration of corticosterone and 18-hydroxycorticosterone (18-OH-B), but not of aldosterone, caused recovery of U-B PCO2 to the level of sham-operated animals treated with amiloride. Aldosterone did not affect U-B PCO2 in the presence of amiloride (21.9 mmHg ADX group vs. 20.98 mmHg aldosterone group). Results are compatible with aldosterone affecting distal H ion secretion mostly by a sodium and potential difference dependent mechanism, while corticosterone and 18-OH-B should act by other mechanisms (e.g., increased luminal buffer level).

18-Hydroxycorticosterone↗
PubMed1991

Bicarbonate reabsorption and electrophysiology of proximal tubules in uninephrectomized rats.

1. The kinetics of acidification of luminal fluid in hypertrophied proximal tubules after unilateral nephrectomy was studied by stationary microperfusion and continuous measurement of luminal pH with antimony microelectrodes. 2. Trans-epithelial and basolateral membrane electrical potential differences were measured in order to detect modifications in electrogenic transport mechanisms under these conditions. 3. The values of stationary pH and HCO3- concentration were significantly lower, the mean acidification half-time was not different and net reabsorptive HCO3- fluxes in proximal tubules were significantly increased in uninephrectomized rats. According to an electrical analogue model, these results suggest (a) a reduction in the internal series resistance of the H+ pump, caused perhaps by an increased density of pump sites, and (b) an increase in the protonmotive force of the pump. 4. The trans-epithelial electrical potential difference measured in free flow conditions was significantly more lumen-positive in uninephrectomized rats. The trans-epithelial electrical potential difference measured during intraluminal perfusion with Ringer solution containing 30 mmol/l HCO3- was significantly more negative in all groups studied. In uninephrectomized rats treated with acetazolamide, the trans-epithelial electrical potential difference was more lumen-negative than that in untreated uninephrectomized rats. These results are compatible with a steeper transepithelial Cl- gradient as well as with electrogenic, active H+ secretion. 5. There was no significant difference in the basolateral electrical potential difference between control and uninephrectomized rats. 6. In conclusion, our data show an increase in the transport rates of HCO3- in the proximal tubule of uninephrectomized rats, which may be due to an increase in the density of transporters in the brush-border membrane, and an increased ability of the transport mechanism to create H+ gradients.

Absorption↗
PubMed1991

Effects of parathyroid hormone on urinary acidification in the rat.

To evaluate the effects of parathyroid hormone (PTH) on urinary acidification parameters, thyroparathyroidectomy was performed in normal (TPTX) and in calcium-supplemented rats (TPTX + Ca2+). Both groups were supplemented with thyroxin. Glomerular filtration rate (GFR) fell from 7.79 +/- 0.33 in the control group (C) to 4.88 +/- 0.26 ml min-1 kg-1 in TPTX, while net acid excretion fell from 5.65 +/- 0.22 in C to 3.76 +/- 0.25 mumol min-1 kg-1 in TPTX. Kinetic data of urinary acidification obtained by microperfusion techniques in proximal tubules showed that the half-time of acidification (t/2) rose from 4.75 +/- 0.24 s in C to 8.97 +/- 0.64 s in TPTX and persisted elevated in TPTX + Ca2+ (7.40 +/- 0.43 s); in the latter group, stationary pH was not significantly different from that of the control group. Bicarbonate reabsorption (JHCO3) fell from 2.18 +/- 0.15 in C to 0.823 +/- 0.082 in TPTX and was 1.53 +/- 0.073 nmol s-1 cm-2 in TPTX + CA2+. These data suggest that normal pH gradients depend on normal calcium levels, but acidification half-times are dependent on PTH, which also contributes to keeping glomerular hemodynamics and acidification rates at normal levels.

Acidosis↗
PubMed1990

pH-stat experiments in proximal renal tubules.

The pH-stat technique has been used to measure H+ fluxes in gastric mucosa and urinary bladder "in vitro" while keeping mucosal pH constant. We now report application of this method in renal tubules. We perfused proximal tubules with double-barreled micropipettes, blocked luminal fluid columns with oil and used a double-barreled Sb/reference microelectrode to measure pH, and Sb or 1 N HC1-filled microelectrodes to inject OH- or H+ ions into the tubule lumen. By varying current injection, pH was kept constant at adjustable levels by an electronic clamping circuit. We could thus obtain ratios of current (nA) to pH change (apparent H(+)-ion conductance). These ratios were reduced after luminal 10(-4) M acetazolamide, during injection of OH-, but they increased during injection of H+. The point-like injection source causes pH to fall off with distance from the injecting electrode tip even in oil-blocked segments. Therefore, a method analogous to cable analysis was used to obtain H+ fluxes per cm2 epithelium. The relation between JH+ and pH gradient showed saturation kinetics of H fluxes, both during OH- and H+ injection. This kinetic behavior is compatible with inhibition of JH by luminal H+. It is also compatible with dependence on Na+ and H+ gradients of a saturable Na/H exchanger. H(+)-ion back-flux into the tubule lumen also showed saturation kinetics. This suggests that H+ flow is mediated by a membrane component, most likely the Na(+)-H+ exchanger.

Acetazolamide↗
PubMed1990

Urinary and proximal tubule acidification during reduction of renal blood flow in the rat.

1. The effects of reduction in renal blood flow (RBF) on urinary acidification and proximal tubule H+ ion secretion were studied after partial aortic clamping in rats. 2. Acute reduction of the renal perfusion pressure (from 109 +/- 3.88 to 77.4 +/- 1.05 mmHg) decreased both inulin and PAH (p-aminohippurate) clearances to about one-third of their control values. Absolute levels of urinary sodium excretion also decreased markedly, but fractional sodium excretion did not change significantly. 3. Urine pH and bicarbonate levels were not affected, but titratable acidity increased significantly from 0.12 +/- 0.011 to 0.25 +/- 0.042 muequiv min-1 ml-1 glomerular filtration rate (GFR). During aortic clamping, cortical PCO2 as determined by means of Severinghaus microelectrodes was reduced by a mean value of 7.0 +/- 1.5 mmHg. 4. Proximal tubule acidification kinetics were studied by stationary microperfusion techniques in which the time course of pH changes was monitored by pH microelectrodes. Steady-state pH fell from a mean control value of 6.77 +/- 0.03 to 6.65 +/- 0.02, and stationary bicarbonate concentrations from 4.70 +/- 0.27 to 2.84 +/- 0.18 mM. Acidification half-time decreased from 5.07 +/- 0.30 to 4.39 +/- 0.19 s, and net bicarbonate reabsorption increased from 1.63 +/- 0.14 to 1.99 +/- 0.12 nmol cm-2 s-1, these changes being statistically significant. 5. The experiments demonstrate that both overall acid excretion and proximal acid secretion are not compromised by a large decrease of RBF to about one-third of the control value; titratable acid excretion and proximal net bicarbonate reabsorption were even moderately increased under these conditions.

Animals↗
PubMed1990

Distal perfusion studies: transport stimulation by native tubule fluid.

It is well established that potassium secretion into the distal tubule increases with the rate of flow. In a previous study [G. Malnic, R. W. Berliner, and G. Giebisch. Am. J. Physiol. 256 (Renal Fluid Electrolyte Physiol. 25): F932-F1271, 1989] we found that the increase with the rate of perfusion with a fluid made up to resemble that normally found in the early distal tubule was substantially less than the increase in free-flow conditions [R. N. Khuri, M. Wiederholt, N. Strieder, and G. Giebisch. Am. J. Physiol. 228: 1249-1261, 1975]. Because of the possibility that some important component was missing from the artificial fluid, we have carried out another series of experiments in which distal tubules were perfused with fluid collected from late proximal tubules and compared the results with those obtained when tubules were perfused with an artificial fluid with an electrolyte composition similar to that of late proximal fluid. When proximal tubule fluid was used, the potassium concentrations in the collected distal fluid were higher and better maintained with increasing flow than when the artificial fluid was used, and consequently the rate of potassium secretion was substantially greater with the proximal tubule fluid, approaching the results of previous studies in free flow. The nature of the component missing from the artificial solution is not known.

Absorption↗
PubMed1990

PCO2 in renal cortex.

In a number of recent investigations a renal cortical PCO2 higher than that of systemic blood was reported. We have studied this problem with the use of micro-Severinghaus electrodes based on antimony, H+ liquid ion exchange, and glass pH electrodes with an inner buffer solution containing 0.5 mg/ml carbonic anhydrase (CA). Measurements in renal cortical structures (renal tubules, star vessels, capillaries, and glomeruli in Munich-Wistar rats) were compared with determinations in renal vein or artery performed with the same electrode in sequence. No significant differences in PCO2 were found between cortical structures and renal vein in control rats, in metabolic alkalosis, respiratory acidosis and alkalosis, and after CA inhibition. Nevertheless, absolute PCO2 levels, which followed the PCO2 of systemic blood, were markedly different in these groups. Measurements of pH and PCO2 at the same tubule site were compatible with HCO3- determinations in tubule fluid in vitro (made with use of the Henderson-Hasselbalch equation) in control rats. When proximal tubules were pump-perfused in vivo with a solution containing 30 mM NaHCO3, measured PCO2 approached that of the perfusing solution at high pump rates, and approached the free-flow value as rates were reduced to zero, indicating that the CO2 generated in the lumen equilibrated rapidly across the epithelium. Reducing renal blood flow by aortic clamping reduced renal cortical PCO2. In conclusion, in a large number of experimental conditions renal cortical PCO2 was never higher than that measured in systemic blood.

Animals↗
PubMed1990

Mechanism of potassium transport across proximal tubule epithelium in the rat.

The mechanism of proximal tubule potassium reabsorption was studied by stopped-flow microperfusion and determination of potassium activities by ion-sensitive resin microelectrodes. The proximal tubule was unable to establish transepithelial potassium gradients. Perfusion with 20 mM K+ turned the lumen 3 mV more negative, an effect abolished by Ba2+. The half-time for K+ activities to reach their stationary level after perfusion with 1 mM K+ was significantly increased by Ba2+ from 4.25 +/- 0.14 s to 11.0 +/- 1.71 s, and after perfusion with 20 mM K+, from 5.43 +/- 0.20 to 12.53 +/- 0.90 s. These data indicate that a significant fraction of potassium is transferred across proximal tubule epithelium by a transcellular, K(+)-channel-dependent route.

Animals↗