Net Potassium Flux Research Articles

Immediate and steady state extracellular ionic fluxes of growing Arabidopsis thaliana root hairs under hyperosmotic and hypoosmotic conditions

Osmotic‐induced shifts in extracellular ionic fluxes at the apex of growing Arabidopsis thaliana L. root hairs were examined using the extracellular self‐referencing (vibrating) ion‐selective probe technique. With either APW 7 (artificial pond water, pH 7) or APW 7 plus 200 mM mannitol/sorbitol, a steady state was reached in which growth rates were the same (0.75 and 0.82 µm min−1) as were the net fluxes of calcium (inward), potassium (outward), and chloride (inward). The outward flux of protons was about 20‐fold larger in APW 7 plus 200 mM mannitol/sorbitol compared to APW 7 (P= 0.028). Significant changes in ionic fluxes within 5 min of osmotic changes were observed for hyperosmotic treatment: a 7.5‐fold increase in the inward calcium flux (P= 0.041) and a 1.7‐fold increase in the outward potassium flux (P= 0.007). Although the change in the calcium flux was consistent with a process of osmotic adjustment (and not a consequence of binding/release from the cell wall), the magnitude of the flux was considerably less than the potassium efflux. Unlike the situation in other organisms where volume regulation explicitly relies upon modulation of ionic fluxes (especially sodium, potassium and chloride), the root hairs may rely on other mechanisms of osmotic regulation, possibly coupled to differences in proton efflux under steady state growth conditions. The root hairs do exhibit an osmotic‐induced electrical signal (R. R. Lew. 1996. Plant Physiol. 112: 1089–1100) which may be a component of initial signal transduction controlling osmotic regulation.

Potassium permeability in the absence of fluid reabsorption in proximal tubule of the anesthetized rat.

A luminal microperfusion technique was used to examine the K+ permeability of surface proximal convoluted tubules (PCT) in the kidney of anesthetized rats. Transtubular potassium concentration ([K+]) gradients were varied by altering the concentration of KCl in luminal perfusates, to which 32 mmol/l of the impermeant solute raffinose was also added to prevent net fluid reabsorption. The arithmetic mean transtubular [K+] gradient was highly predictive of net potassium flux, yielding an apparent K+ permeability of 31.9 +/- 1.7 x 10(-5) cm/s in the absence of fluid reabsorption. When compared using identical calculation techniques, we found this was not significantly different from the permeability derived in a previous study when fluid reabsorption was present [J. D. Kibble, M. Wareing, R. W. Wilson, and R.Green. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 27): F778-F783, 1995]. We conclude that fluid reabsorption does not affect the apparent permeability of the proximal tubule to potassium. The apparent permeability to 86Rb, measured following its addition to luminal perfusates, was not significantly different from the value obtained for K+, suggesting that rubidium is a useful marker for net potassium movements in the PCT of the rat.

The role of active transport in potassium reabsorption in the proximal convoluted tubule of the anaesthetized rat.

1. We have previously assessed the contributions of diffusion and convection to net potassium reabsorption in the rat proximal convoluted tubule (PCT). The present study was conducted to evaluate the role of active transport in convective potassium reabsorption by measuring the transepithelial potassium reflection coefficient (sigmaK) in the presence and absence of cyanide in anaesthetized rats previously prepared for in vivo microperfusion. 2. Osmotic water permeability (Pf) was measured in double-perfused tubules (lumen and peritubular capillaries) by manipulating the applied transepithelial osmotic gradient between -30 and +40 mosmol (kg H2O)(-1) using raffinose added to or subtracted from luminal perfusates. Pf was unaffected by the presence of cyanide when the estimated dissipation of osmotic gradients along each tubule were taken into account. 3. The proportion of K+ (and Na+) convectively transported with water fluxes (i.e. sigmaK) was not affected by cyanide. In the absence of active transport and following correction for any diffusive component, sigmaK was 0.56 +/- 0.13, indicating substantial solvent drag which probably occurs via the paracellular pathway. 4. However, cyanide caused a reduction in net potassium flux over the entire range of fluid fluxes used in double-perfusion experiments. Subsequent single-perfusion experiments (tubule lumen only) using the specific K+-H+-ATPase inhibitor, SCH28080, failed to reveal any direct evidence for a primary active K+ transporting mechanism involved in K+ reabsorption in the PCT.

Effects of glucocorticoid and mineralocorticoid on potassium transport in the rat medullary thick ascending limb of Henle's loop

Potassium transport in the thick ascending limb is conducted by heterogeneous cells to opposite directions. Effects of glucocorticoids and mineralocorticoids on potassium transport of the rat medullary thick ascending limb (MTAL) were examined by in vitro microperfusion technique by measuring net potassium flux (JK), and apparent potassium conductances in the apical and basolateral membranes of two cell populations. Segments of MTAL were obtained from four groups of rats: sham operated control rats, adrenalectomized rats (ADX), adrenalectomized rats treated with dexamethasone (DEX), and adrenalectomized rats treated with aldosterone (ALDO). Fractional urinary potassium excretion was reduced by ADX and partially recovered by either DEX or ALDO. JK of the isolated perfused MTAL was markedly decreased by ADX from 5.13 to 1.94 pmol/min/mm. It was partially recovered by DEX (3.36 pmol/min/mm), but not by ALDO (2.07 pmol/min/mm). Random impalement of MTAL cells with a microelectrode in the control group revealed two cell populations; 76% was high basolateral conductance cell (HBC) and 24% was low basolateral conductance cell (LBC). In the ADX group, the basolateral potassium conductance of the HBC cell was markedly reduced, whereas the apical membrane potassium conductance of the HBC cell was increased. These changes were recovered in the DEX group, but not in the ALDO group. Potassium conductances of the apical and basolateral membranes in the LBC were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Reconstitution and partial purification of the glibenclamide-sensitive, ATP-dependent K+ channel from rat liver and beef heart mitochondria.

The transport properties of mitochondria are such that net potassium flux across the inner membrane determines mitochondrial volume. It has been known that K+ uptake is mediated by diffusive leak driven by the high electrical membrane potential maintained by redox-driven, electrogenic proton ejection and that regulated K+ efflux is mediated by an 82-kDa inner membrane K+/H+ antiporter. There is also long-standing suggestive evidence for the existence of an inner membrane protein designed to catalyze electrophoretic K+ uptake into mitochondria. We report reconstitution of a highly purified inner membrane protein fraction from rat liver and beef heart mitochondria that catalyzes electrophoretic K+ flux in liposomes and channel activity in planar lipid bilayers. The unit conductance of the channel at saturating [K+] is about 30 pS. Reconstituted K+ flux is inhibited with high affinity by ATP and ADP in the presence of divalent cations and by glibenclamide in the absence of divalent cations. The mitochondrial ATP-dependent K+ channel is selective for K+, with a Km of 32 mM, and does not transport Na+. K+ transport depends on voltage in a manner consistent with a channel activity that is not voltage-regulated. Thus, the mitochondrial ATP-dependent K+ channel exhibits properties that are remarkably similar to those of the ATP-dependent K+ channels of plasma membranes.

Permeability of fetal microvessels in the perfused term human placenta

The toxicity of calcium ethylenediaminetetraacetate (CaEDTA) resulting from sustained iv infusion was studied in dogs. Signs of toxicity included vomiting, depression, and, occasionally, bloody diarrhea. The dogs were in a shocklike state terminally. Because of the reported nephrotoxicity of the drug, parameters of renal function were measured using conventional steady-state techniques. Glomerular filtration rate, renal plasma flow, and tubular maxima for glucose and PAH were decreased 8–22% following CaEDTA infusion; acetate enhancement of TmPAH was substantially reduced. Essentially no changes occurred in blood urea nitrogen, plasma electrolyte concentrations, or urinary excretion rates of sodium, potassium, or chloride. Histopathologic changes included hemorrhage and necrosis of intestinal epithelium with loss of villous structure and a necrotizing nephrosis of the proximal convoluted tubules.Evaluation of intestinal function revealed a marked depression of glucose absorption but no significant changes in the net fluxes of sodium, potassium, or chloride from the duodenum as toxicity developed. The permeability of the intestine to a volume marker was greatly increased. Studies of the intestinal diffusion ratios of solutes of various molecular sizes indicated the permeability increase was limited to the relatively large molecules.The results indicate CaEDTA is not primarily nephrotoxic in the dog and, therefore, renal failure probably is not the cause of death. The infusion of a very stable chelate, CrEDTA, was nontoxic. This suggested that CaEDTA toxicity is due to its chelative properties rather than some nonspecific action of the EDTA moiety.

Effect of maternal hypokalaemia on unidirectional maternofetal and net potassium fluxes across the placenta of the anaesthetized rat

Potassium (K +)fluxes across the placenta of rats, at 21 days gestation, fed a low K + diet or a control diet were studied. The rats on the low K + diet had a significantly ( P < 0.001) lower arterial plasma K + concentration compared to those on the control diet (1.95 ± 0.12 and 2.93 ± 0.06 mmol/l respectively; mean ± s. e., n = 17). Fetal umbilical arterial plasma K + concentration was unaltered in maternal hypokalaemia and was significantly ( P<0.001) higher than that of maternal plasma (4.58 ± 0.15 and 4.66 ± 0.12 mmol/l in low K + and control groups respectively). Net K + flux across the placentas (as measured by fetal accretion between days 20 and 21 of gestation) of hypokalaemic mothers (0.106 ± 0.02 μmol/min/g placenta, n = 6) was not different to that in controls (0.104 ± 0.01 μmol/min/g placenta, n = 8). Unidirectional maternofetal flux ( J mf) across the placentas, measured as the accumulation of 42K in the fetuses after injection of the radioisotope into maternal blood, was also not significantly different between the hypokalaemic and control mothers (0.5 ± 0.08 μmol/min/g placenta, n = 8 versus 0.63 ± 0.06 μmol/min/g placenta, n = 7, respectively). However, measurement of J mf by perfusion of the placentas through their fetal circulations yielded a higher value than the accumulation method and in this analysis was significantly ( P < 0.02) lower in the low K + than in the control group (0.75 ± 0.1O μmol/min/g placenta, n = 11, and 1.27 ± 0.14 μmol/min/g placenta, n = 9, respectively). These results show that net placental K + fluxes are unaltered during maternal hypokalaemia but suggest that unidirectional maternofetal fluxes may be reduced.

Accumulation of potassium and calcium in rat myocardium exposed to alpha-1-adrenoceptor stimulation.

Net fluxes of potassium, calcium, sodium and chloride were examined in isolated perfused rat hearts during alpha-1-adrenoceptor stimulation. The ion measurements were performed in the non-recirculating perfusate. Hearts were exposed to alpha-1-adrenoceptor stimulation (phenylephrine 5 x 10(-5) mol/l in the presence of the beta-blocker timolol 10(-6) mol/l). During alpha-1-adrenoceptor stimulation perfusate potassium fell relatively rapidly by about 0.10 mmol/l after approximately 100 sec. followed by a slower rise. About 180 sec. after onset of alpha-1-adrenoceptor stimulation, the potassium level was about 0.06 mmol/l below the control concentration level. This reduction was eliminated by the alpha-1-adrenoceptor blocker prazosin (10(-7) mol/l). The effects on net calcium fluxes were measured at two different calcium concentrations. For both concentrations we found a small but statistically significant reduction of the calcium concentration in the perfusate after alpha-1-adrenoceptor stimulation. Neither sodium nor chloride perfusate concentrations showed statistical significant changes compared to control values. The present observations revealed the existence of alpha-1-adrenoceptor regulated mechanisms related to a net uptake of both potassium and calcium in rat heart.

Dicyclohexylcarbodiimide reacts specifically with the 16kDa subunit of larval Manduca sexta midgut vacuolar-type ATPase.

ABSTRACT Proton-motive vacuolar-class ATPases (V-ATPases) are commonly associated with membrane-bound organelles other than mitochondria and chloroplasts. They are found in the vacuoles of Neurospora crassa and yeasts, in tonoplasts of plants and in endomembranes such as lysosomes, endosomes, clathrin-coated vesicles and secretory granules (Sze, 1985; Rudnick, 1986; Mellman et al. 1986; Rodman et al. 1991). However, they have also been found in plasma membranes of kidney tubules (Brown et al. 1987; Wang and Gluck, 1990). Recently, the pump responsible for the large lumen-directed net flux of potassium across larval Manduca sexta midgut has been shown to consist of a plasma membrane protonmotive V-ATPase functioning in conjunction with an nH+/K+ antiporter (Wieczorek et al. 1991).

Active potassium absorption by the renal distal tubule.

Maintenance of potassium homeostasis during potassium depletion appears to involve an active potassium absorptive mechanism in the distal nephron. Direct demonstration of such a pathway in the distal tubule of the rat has been lacking. The purpose of the current study was to examine the hypothesis that an ATP-dependent active transport mechanism plays a role in potassium absorption by the rat distal tubule. We utilized in vivo microperfusion techniques in Sprague-Dawley rats maintained on a regular diet of low-potassium diet for 3-4 wk. The effect of a selective inhibitor of the gastric H-K-adenosinetriphosphatase (ATPase) (Sch 28080, 0.1 mM) was tested in distal tubules of both groups of rats. Distal tubules of normal rats secreted potassium. Sch 28080 had no effect on this net potassium flux. In contrast, distal tubules of potassium-deficient rats absorbed potassium. Sch 28080 abolished this potassium absorption and produced a small hyperpolarization of the lumen-negative transepithelial voltage (VTE). The change in VTE can be explained by a concomitant increase in potassium concentration in the late distal tubule. These results are consistent with the presence of an H-K-ATPase in the distal tubule of potassium-deficient rats.

Net basolateral potassium flux and short-circuit current in ouabain-treated frog skin

A new technique has been developed to correlate K loss from cells (JK) across the basolateral membrane into a K-free ouabain Ringer solution and short-circuit current (Isc) for a model Na-transporting epithelium, the frog skin. Distinct differences were observed when the tissue was bathed in sulfate or chloride Ringer. In sulfate Ringer, K-free ouabain treatment caused both JK and Isc to decline in a nearly parallel fashion with time. JK-Isc was approximately 1 microA/cm2. In sulfate Ringer, isoproterenol caused parallel increases, whereas amiloride (apical side) caused parallel decreases in JK and Isc. In chloride Ringer, K-free ouabain treatment caused Isc to decline at a slightly faster rate than JK.JK-Isc was approximately 8 microA/cm2. Bumetanide decreased JK with very little effect on Isc. Barium caused small parallel changes in both Isc and JK. Amiloride decreased Isc with very little effect on JK. These experiments show that after ouabain treatment changes in JK from the cells across the basolateral membrane can largely account for changes in Isc. However, JK also occurs via neutral mechanisms and perhaps from cells not related to the transport pathway, demonstrating that there is not always a tight coupling of K loss at the basolateral membrane with Na entry across the apical membrane.

Luminal calcium regulates potassium transport by the renal distal tubule

We examined the effect of changes in lumen calcium concentration on net potassium transport by distal tubules in anesthetized rats. Tubules were perfused with a control solution that resembled interstitial fluid but lacked calcium. Experimental solutions were prepared by adding varying amounts of CaCl2 to the control solution to produce solutions with free ionic calcium concentration ([Ca2+]) of 0.2, 0.4, and 0.8 mM. In paired comparisons 0.2 mM Ca2+ did not affect net potassium transport, whereas 0.4 and 0.8 mM Ca2+ each reduced potassium secretion by approximately 30%. Unidirectional potassium fluxes using 86Rb as a tracer for potassium and transepithelial voltage (VTE) were measured to characterize further the effect of calcium on potassium transport. Presence of 0.8 mM Ca2+ in the lumen did not affect unidirectional absorptive potassium flux; therefore, the decrease in net potassium flux was accounted for entirely by a decrease in unidirectional secretory potassium flux. The lumen negative VTE measured in the late distal tubule decreased during perfusion with 0.8 mM Ca2+. These results are consistent with the hypothesis that increases in lumen (extracellular) calcium concentration in the range normally present in the distal tubule reduce net potassium secretion by decreasing the electrochemical gradient for potassium secretion.

Modulation of active potassium transport by aldosterone

1. 1. The role of aldosterone on active potassium transport across lizard colon under voltage-clamped conditions has been investigated. 2. 2. Control colons exhibited no net potassium flux ( J k net ) despite of the existence of active opposite unidi ectional fluxes. 3. 3. An important net secretory potassium flux was found in short-circuited aldosterone-stimulated colons. 4. 4. Mucosal amiloride did not change ( J k net) either in control or aldosterone-stimulated colons. 5. 5. Luminal barium alters K + transport in a manner consistent with the presence of barium-sensitive conductances at the apical membrane of both control and aldosterone-treated colons. 6. 6. The effects of ouabain and barium on control and aldosterone-induced potassium flows were consistent with a model involving basolateral uptake by an Na +-K +-ATPase and conductive exit across the apical membrane. 7. 7. The stimulatory effect of aldosterone on potassium secretion is associated with parallel increases of both basolateral K + entry and the apical conductive pathway.

Effects of gastric fundic stimulation on glucose absorption and water and electrolyte fluxes from rabbit small bowel.

A single-pass perfusion model was developed to measure net fluxes of glucose, water, sodium, and potassium across upper jejunal and duodenal mucosa in vivo in the anaesthetised rabbit. Irrigation of the gastric fundic mucosa with Michaelis' buffer (pH 8) reduced jejunal mean glucose absorption by 21.3% (P less than 0.04) and duodenal glucose absorption by 27.2%. Irrigation of gastric fundic mucosa with 0.1 M glycine at pH 2 increased mean jejunal glucose absorption by 25%. Jejunal net secretion of water and sodium were reduced by gastric fundic alkali. Potassium net fluxes in jejunum and duodenum were not significantly affected. These results support the hypothesis that the gastric fundic mucosa is sensitive to chemical stimulation, responding by a humoral mechanism that modified the rate of glucose absorption from the small bowel mucosa.

Effects of muscarinic, alpha-adrenergic, and substance P agonists and ionomycin on ion transport mechanisms in the rat parotid acinar cell. The dependence of ion transport on intracellular calcium.

The relationship between receptor-mediated increases in the intracellular free calcium concentration [( Ca]i) and the stimulation of ion fluxes involved in fluid secretion was examined in the rat parotid acinar cell. Agonist-induced increases in [Ca]i caused the rapid net loss of up to 50-60% of the total content of intracellular chloride (Cli) and potassium (Ki), which is consistent with the activation of calcium-sensitive chloride and potassium channels. These ion movements were accompanied by a 25% reduction in the intracellular volume. The relative magnitudes of the losses of Ki and the net potassium fluxes promoted by carbachol (a muscarinic agonist), phenylephrine (an alpha-adrenergic agonist), and substance P were very similar to their characteristic effects on elevating [Ca]i. Carbachol stimulated the loss of Ki through multiple efflux pathways, including the large-conductance Ca-activated K channel. Carbachol and substance P increased the levels of intracellular sodium (Nai) to more than 2.5 times the normal level by stimulating the net uptake of sodium through multiple pathways; Na-K-2Cl cotransport accounted for greater than 50% of the influx, and approximately 20% was via Na-H exchange, which led to a net alkalinization of the cells. Ionomycin stimulated similar fluxes through these two pathways, but also promoted sodium influx through an additional pathway which was nearly equivalent in magnitude to the combined uptake through the other two pathways. The carbachol-induced increase in Nai and decrease in Ki stimulated the activity of the sodium pump, measured by the ouabain-sensitive rate of oxygen consumption, to nearly maximal levels. In the absence of extracellular calcium or in cells loaded with the calcium chelator BAPTA (bis[o-aminophenoxy]ethane-N,N,N',N'-tetraacetic acid) the magnitudes of agonist- or ionomycin-stimulated ion fluxes were greatly reduced. The parotid cells displayed a marked desensitization to substance P; within 10 min the elevation of [Ca]i and alterations in Ki, Nai, and cell volume spontaneously returned to near baseline levels. In addition to quantitating the activation of various ion flux pathways in the rat parotid acinar cell, these results demonstrate that the activation of ion transport systems responsible for fluid secretion in this tissue is closely linked to the elevation of [Ca]i.

Factors controlling the chemical alteration of throughfall in a subalpine balsam fir canopy

Rainfall and throughfall (TF) at four canopy levels were collected sequentially during four storms in a subalpine balsam fir forest on Mount Moosilauke, New Hampshire. The chemical compositions of throughfall (TF) and “net TF” (rainfall concentrations subtracted from TF concentrations) were compared with precipitation chemistry, amounts and intensities. Net TF fluxes of ammonium, nitrate, hydrogen, potassium and sulfate ions were influenced by concentration gradients between TF and the canopy. For ions taken up by the canopy, there was less uptake at lower rainfall concentrations, and for those released, there was less loss at higher rainfall concentrations. For all these ions, the effect of concentration gradients between surface water and canopy component internal pools was also suggested by the fact that most of the release (or uptake for ammonium and nitrate) occurred on components located high in the canopy. On these components, concentration differences between TF and canopy component internal pools should be greatest. Next TF concentrations of ammonium and nitrate approached zero with cumulative precipitation, indicating that the mechanisms through which the canopy takes up these ions became saturated. Diffusion driven by concentration gradients between TF at canopy surfaces and the interiors of foliage and other canopy components is consistent with these observations. Hydrogen and potassium ions were released to TF water from canopy component surfaces. These losses from canopy components declined with cumulative precipitation, apparently by depletion of internal sources of ions. Sulfate ions were also apparently always released by this canopy to throughfall, and sulfate is the only ion considered in this study which showed a positive effect of rainfall intensity on the magnitude of ionic release from canopy components.

Effect of adrenalectomy on transport in the rat medullary thick ascending limb.

Previous studies in adrenalectomized (Adx) rats suggest that aldosterone may regulate ion transport in the ascending portion of Helen's loop. In order to examine directly the effect of adrenalectomy on transport, medullary thick ascending limb (Mtal) segments were isolated from Adx, Adx replaced with aldosterone (Adx + Ald, 0.5 micrograms X 100 g X body wt X d), and control Sprague-Dawley rats. Both net sodium and net chloride fluxes were significantly less in the Mtal segments from Adx rats compared with those in the control or Adx + Ald group. Physiologic levels of exogenous aldosterone increased net sodium chloride flux toward control values in the Adx + Ald group. Net potassium flux was not different among the three groups. We conclude that adrenalectomy impairs reabsorptive NaCl but not K transport in the Mtal, and that aldosterone restores this process. This reabsorptive defect may contribute to the urinary concentrating and diluting abnormality associated with adrenal insufficiency.

K transport in upper portion of descending limbs of long-loop nephron from hamster.

By use of the in vitro microperfusion technique, we investigated potassium transport in the upper portion of the descending limb of the long-loop nephron isolated from hamster kidney. The net potassium flux determined by ultramicro-flame photometry was -0.63 +/- 1.84 pmol X mm-1 X min-1, a value that was not significantly different from zero. The salt permeability for KCl was calculated from the amount of potassium entering the tubular lumen when the concentration of potassium in the bath was increased by approximately 5 mM. The value was 38.9 +/- 1.9 X 10(-5) cm X s-1. The bidirectional fluxes of 86Rb were measured as indices of potassium fluxes. Flux coefficients from lumen-to-bath and bath-to-lumen were 51.2 +/- 9.2 and 48.8 +/- 13.5 X 10(-5) cm X s-1, respectively. These values were not significantly different, confirming that there was no net flux for 86Rb. In another series of five experiments, the lumen-to-bath 86Rb flux coefficients were 69.4 +/- 13.2 X 10(-5) cm X s-1 in the absence of unlabeled Rb, and 70.2 +/- 13.9 X 10(-5) cm X s-1 in the presence of 5 mM unlabeled Rb. The lumen-to-bath 42K flux coefficient measured in the same series of animals was 85.3 +/- 10.5 X 10(-5) cm X s-1 (n = 10), a value that is slightly higher than, but not significantly different from, that of 86Rb. These data show that active potassium transport may exist in this segment and that the passive permeability for potassium is very high.(ABSTRACT TRUNCATED AT 250 WORDS)

Unidirectional potassium fluxes in renal distal tubule: effects of chloride and barium.

Low luminal concentrations of chloride stimulate net potassium secretion by the renal distal tubule, independent of changes in transepithelial voltage. These effects are not prevented by the luminal application of the potassium channel blocking agent barium. Because net potassium secretion comprises secretory and absorptive components, we sought to evaluate the effects of chloride and barium on unidirectional potassium fluxes in the renal distal tubule. In vivo microperfusion methods were used in anesthetized Sprague-Dawley rats. Perfusion solutions contained either 42K or 86Rb as tracers for potassium. Tracer efflux coefficients, indicating apparent potassium permeability, were similar when measured using either isotope. Net potassium flux was determined as the difference between perfusion and collected rate, and unidirectional absorptive potassium flux was calculated as the product of the mean luminal potassium concentration and the tracer efflux coefficient. During perfusion with a solution that resembled fluid normally arriving at the early distal tubule, the absorptive potassium flux was approximately 25% of the unidirectional secretory flux. Reducing lumen chloride concentration increased net potassium secretion, because blood-to-lumen potassium flux increased from 61 +/- 12.7 to 96 +/- 14.6 pmol/min. Barium reduced both absorptive and secretory fluxes but did not prevent the stimulation of net potassium secretion that occurs when luminal chloride concentration is reduced. Apparent potassium permeability during perfusion with a solution that resembled fluid normally arriving at the early distal tubule was 800 nm/s when corrected for voltage. Together with the results of previous experiments, these results are consistent with the presence of a secretory pathway linking potassium with chloride in the luminal membrane of cells of the distal tubule.

ECTOMYCORRHIZAS AFFECT IONIC BALANCE DURING AMMONIUM UPTAKE BY DOUGLAS‐FIR ROOTS

SUMMARYMycorrhizas have been shown to alter ion fluxes for many nutrients. Experiments were done to determine the extent to which ectomycorrhizas alter the ionic balance of roots of Douglas‐fir (Pseudotsuga menziesii (Mirb.) Franco) seedlings mycorrhizal with Hebeloma crustuliniforme (Bull, ex St. Amans) Qúel. exposed to solutions containing either 16N ammonium sulphate or 16N ammonium chloride. Net fluxes of ammonium, hydrogen, potassium, calcium, sodium, bicarbonate, sulphate and chloride were measured. The mycorrhizal association altered ion fluxes, primarily decreasing sodium uptake and potassium release rates (both anion treatments) and increasing bicarbonate release during exposure to ammonium chloride. Rates of carboxylate accumulation in the tissue were inferred from the net flux data; mycorrhizal seedlings may produce more cation‐carboxylate complexes compared with nonmycorrhizal seedlings. When compared with agricultural plants exposed to ammonium, Douglas‐fir took up a considerably greater number of cations for each ammonium ion absorbed, which may account for the greater number of carboxylate anions also produced by Douglas‐fir. These findings were discussed in terms of ecological significance for growth of Douglas‐fir.