Net Potassium Transport Research Articles

Silicon deposition in the root reduces sodium uptake in rice (Oryza sativa L.) seedlings by reducing bypass flow

Sodium chloride reduces the growth of rice seedlings, which accumulate excessive concentrations of sodium and chloride ions in their leaves. In this paper, we describe how silicon decreases transpirational bypass flow and ion concentrations in the xylem sap in rice (Oryza sativa L.) seedlings growing under NaCl stress. Salt (50 mM NaCl) reduced the growth of shoots and roots: adding silicate (3 mM) to the saline culture solution improved the growth of the shoots, but not roots. The improvement of shoot growth in the presence of silicate was correlated with reduced sodium concentration in the shoot. The net transport rate of Na from the root to shoot (expressed per unit of root mass) was also decreased by added silicate. There was, however, no effect of silicate on the net transport of potassium. Furthermore, in salt-stressed plants, silicate did not decrease the transpiration, and even increased it in seedlings pre-treated with silicate for 7 d prior to salt treatment, indicating that the reduction of sodium uptake by silicate was not simply through a reduction in volume flow from root to shoot. Experiments using trisodium-8-hydroxy-1,3,6-pyrenetrisulphonic acid (PTS), an apoplastic tracer, showed that silicate dramatically decreased transpirational bypass flow in rice (from about 4.2 to 0.8%), while the apparent sodium concentration in the xylem, which was estimated indirectly from the flux data, decreased from 6.2 to 2.8 mM. Direct measurements of the concentration of sodium in xylem sap sampled using Philaenus spumarius confirmed that the apparent reduction was not a consequence of sodium recycling. X-ray microanalysis showed that silicon was deposited in the outer part of the root and in the endodermis, being more obvious in the latter than in the former. The results suggest that silicon deposition in the exodermis and endodermis reduced sodium uptake in rice (Oryza sativa L.) seedlings under NaCl stress through a reduction in apoplastic transport across the root.

Effects of ATP-sensitive potassium channel opener on potassium transport and alveolar fluid clearance in the resected human lung.

Since the effect of an ATP-sensitive potassium channel (KATP channel) opener on the function of alveolar epithelial cells is unknown, the effect of YM934, a newly synthesized KATP channel opener, on potassium influx into the alveolar spaces and alveolar fluid clearance was determined in the resected human lung. An isosmolar albumin solution with a low potassium concentration was instilled into the distal airspaces of resected human lungs. Alveolar fluid clearance was measured by the progressive increase in alveolar protein concentration. Net potassium transport was measured by the change in potassium concentration and alveolar fluid volume. YM934 (10(-4) M) increased net influx of potassium by 140% into the alveolar spaces and also increased alveolar fluid clearance by 60% in the experiments with a potassium concentration of 0.3 mEq/1. Glibenclamide (10(-4) M), a KATP channel blocker, inhibited the YM934-increased influx of potassium transport and the increase in alveolar fluid clearance. Also amiloride (10(-5) M), an inhibitors of apical sodium uptake, blocked the YM934 stimulated increase in net alveolar fluid clearance. These results indicate that a KATP channel opener can effect potassium transport and net vectorial fluid movement across the human alveolar epithelium.

Effect of barium on potassium diffusion across the proximal convoluted tubule of the anesthetized rat.

The role of diffusion in transepithelial potassium flux and the importance of potassium channels in the luminal cell membrane to this process were examined by applying a luminal microperfusion technique to surface tubules in kidneys of anesthetized rats. Potassium concentration gradients were applied by altering the concentration of KCl in perfusates. To some perfusates, 2 mmol/l BaCl2 was added to block potassium channels in the luminal cell membrane. The mean applied potassium concentration gradient was highly predictive of net potassium transport in the absence of any change in fluid reabsorption, with an apparent potassium permeability of 22 x 10(-5) cm/s. Thus potassium transport in the proximal tubule may have an important diffusive component. Luminal barium significantly reduced the concentration of potassium in collected fluid under conditions of net potassium secretion, although a substantial barium-insensitive potassium permeability was also observed. However, the site of action of luminally applied barium is uncertain in proximal tubule, since barium was reabsorbed by the tubule at a rate of 13.6 pmol.mm-1.min-1. We conclude that diffusion is a significant driving force for potassium reabsorption in proximal tubule and that most diffusive potassium transport occurs via a barium-insensitive route, possibly the paracellular pathway.

Functional adaptation of rat remnant colon after proximal hemicolectomy

Functional adaptation of the remnant intestine after extensive resection of small bowel is well documented. The effects of partial resection of large bowel on the remaining colon have not been characterized. Transepithelial potential (VT), tissue resistance (RT), and short-circuit current (Isc) were measured in vitro across distal colonic tissue of rats three weeks after proximal hemicolectomy with ileotransversotomy and compared to the same parameters measured in the distal colon of control animals. In a second series of experiments, an in vivo perfusion technique was used to measure changes in sodium, potassium, and water transport in distal colon following proximal hemicolectomy. A 2.5-fold increase in VT (P less than 0.01), a 62% increase in RT (P less than 0.001), and a 35% increase in Isc (P less than 0.05) were observed three weeks following hemicolectomy when compared to control animals. A 64% increase in net sodium absorption (P less than 0.025), no significant change in net potassium transport, and a 115% increase in net water absorption (P less than 0.01) were demonstrated in hemicolectomized animals when compared to control. It is concluded that in the rat the distal colon is capable of functional adaptation to increase net sodium and water absorption within three weeks after proximal hemicolectomy. The mechanism responsible for this adaptive process has yet to be defined. Our findings may explain the lack of chronic diarrhea in patients undergoing right hemicolectomy.

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.

Effect of vasopressin analogue (dDAVP) on potassium transport in medullary collecting duct.

The microcatheterization technique was used to examine electrolyte transport in the medullary collecting duct of two groups of anesthetized rats during water diuresis and during a second experimental phase with 1-desamino-8-D-arginine vasopressin (dDAVP) administration or continued water diuresis. Potassium reabsorption of 53-61% of the delivered load was consistently observed in the medullary collecting duct during water diuresis. During dDAVP administration, urinary potassium excretion doubled, and there was no net potassium transport (reabsorption or secretion) in the medullary collecting duct. The change in potassium transport in medullary collecting duct from water diuresis to antidiuresis (dDAVP) was sufficient to account for the increase in urinary potassium excretion. Changes in flow rate, luminal sodium concentration, or collecting duct sodium reabsorption could not account for the changes in potassium transport in the collecting duct during dDAVP. The results are interpreted as indicating that dDAVP stimulates potassium entry (secretion) into the medullary collecting duct, probably by a direct effect. This action of antidiuretic hormone appears to be important in maintaining potassium homeostasis during changing water balance.

Control of sodium and potassium transport in the cortical collecting duct of the rat. Effects of bradykinin, vasopressin, and deoxycorticosterone.

Several factors interact to maintain precise control of electrolyte transport in the mammalian cortical collecting duct. We have studied the effects of deoxycorticosterone, arginine vasopressin, and bradykinin on net transepithelial sodium and potassium transport in isolated, perfused rat cortical collecting ducts. Chronic administration of deoxycorticosterone to rats increased both sodium absorption and potassium secretion above very low basal levels. Consequently, deoxycorticosterone-treated rats were used for all remaining studies. Arginine vasopressin (10(-10) M in the bath) caused a sustained fourfold increase in net sodium absorption and a sustained threefold increase in net potassium secretion. Bradykinin (10(-9) M in the bath) caused a reversible 40-50% inhibition of net sodium absorption without affecting net potassium transport or the transepithelial potential difference. In the perfusate, up to 10(-6) M bradykinin had no effect. We conclude: As in rabbits, chronic deoxycorticosterone administration to rats increases sodium absorption and potassium secretion in cortical collecting ducts perfused in vitro. Arginine vasopressin causes a reversible increase in net potassium secretion and net sodium absorption. Bradykinin in the peritubular bathing solution reversibly inhibits net sodium absorption, possibly by affecting an electroneutral sodium transport pathway.

Reversal of net secretion to net absorption of potassium in rat large intestine by dietary potassium depletion.

Feeding rats a diet low in potassium and high in sodium for 2 weeks led to a reversal of net potassium secretion to net potassium absorption in ligated segments of distal large intestine (colon descendens and rectum) under in-vivo conditions. This change in the direction of net potassium transport is probably important for the maintenance of potassium homeostasis.

Effect of norepinephrine on swelling-induced potassium transport in duck red cells. Evidence against a volume-regulatory decrease under physiological conditions.

Duck red cells exhibit specific volume-sensitive ion transport processes that are inhibited by furosemide, but not by ouabain. Swelling cells in a hypotonic synthetic medium activates a chloride-dependent, but sodium-independent, potassium transport. Shrinking cells in a hypertonic synthetic medium stimulates an electrically neutral co-transport of [Na + K + 2 Cl] with an associated 1:1 K/K (or K/Rb) exchange. These shrinkage-induced modes can also be activated in both hypo- and hypertonic solutions by beta-adrenergic catecholamines (e.g., norepinephrine). Freshly drawn cells spontaneously shrink approximately 4-5% when removed from the influence of endogenous plasma catecholamines, either by incubation in a catecholamine-free, plasma-like synthetic medium, or in plasma to which a beta-receptor blocking dose of propranolol has been added. This spontaneous shrinkage resembles the response of hypotonically swollen cells in that it is due to a net loss of KCl with no change in cell sodium. Norepinephrine abolishes the net potassium transport seen in both fresh and hypotonically swollen cells. Moreover, cells swollen in diluted plasma, at physiological pH and extracellular potassium, show no net loss of KCl and water ("volume-regulatory decrease") unless propranolol is added. Examination of the individual cation fluxes in the presence of catecholamines demonstrates that activation of [Na + K + 2Cl] co-transport with its associated K/Rb exchange prevents, or overrides, swelling-induced [K + Cl] co-transport. These results, therefore, cast doubt on whether the swelling-induced [K + Cl] system can serve a volume-regulatory function under in vivo conditions.

Role of Aldosterone and Dietary Potassium in Potassium Adaptation in the Distal Colon of the Rat

The present experiments were designed to differentiate the effects of aldosterone and chronic potassium loading in the mechanism of colonic potassium adaptation, using a recently described animal model that permits systematic manipulation of aldosterone and dietary potassium. Unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal colonic mucosa from rats with intact adrenal glands and in adrenalectomized, hormone-replaced animals. Administration of a potassium-enriched diet reversed net potassium absorption (+0.43 +/- 0.10 muEq/h.cm2) in intact animals to net potassium secretion (-0.76 +/- 0.08 muEq/h.cm2). Infusion of aldosterone in adrenalectomized animals, in an amount equivalent to that produced by potassium loading in intact rats, reduced JnetK to zero (-0.03 +/- 0.06 muEq/h.cm2). Similarly, zero net potassium transport (-0.14 +/- 0.08 muEq/h.cm2) was observed when experimental rats were fed a potassium-enriched diet and maintained with basal aldosterone levels. Therefore, both elevated aldosterone levels and a potassium-enriched diet had an effect on net potassium transport, but neither produced the full effects of chronic potassium loading. An increase in net potassium secretion (-0.57 +/- 0.07 myEq/h.cm2) comparable to that of intact potassium-loaded animals did, however, occur when potassium loading and elevated aldosterone levels were combined in experimental animals. These studies demonstrate that (a) chronic potassium loading alters active potassium transport by an aldosterone-independent mechanism and (b) the mechanism of chronic potassium adaptation represents the additive effects of increased dietary potassium and aldosterone.

Potassium transport in the isolated pharate pupal integument of the tobacco hornworm,Manduca sexta

Molting fluid accumulates in the exuvial space beneath the old cuticle between 24 and 12 h before the larval-pupal ecdysis in pharate pupae ofManduca sexta. Just before the molt (9 to 3 h), however, molting fluid disappears from the exuvial space. The integument separates the molting fluid (K+=140 mM) from the hemolymph (K+=35 mM). We have studied potassium transport across isolated, short-circuited preparations of the integument. In 32 mM potassium saline, potassium is actively transported in the hemolymph to exuvial direction at 0.27 and 0.34 μEq cm−2h−1 in preparations isolated at 15 and 6 h before the molt, respectively. The open-circuit potential difference (exuvial side positive) is 5.6 and 14.4 mV at 15 and 6 h before the molt, respectively. The short-circuit current, which can be accounted for by net potassium transport at 15 h before the molt, can not be completely accounted for by net potassium transport at 6 h before the molt (short-circuit current is 7.5 and 13 μA cm−2 at 15 and 6 h before the molt, respectively). At 15 h before the molt the values forKm andJmax are 15.2 mM and 0.4 μEq cm−2 h−1 and at 6 h before the molt these values are 32 mM and 0.7 μEq cm−2 h−1. The short-circuit current is not inhibited by ouabain, thallous ions, and acetazolamide, but is inhibited by 100% N2. During the period between 15 and 6 h before the molt, the integument undergoes a number of developmental changes. These are reflected in the tanning of the cuticle, the changes in the electrical properties, such as the increase in resistance, and the changes in the kinetic properties of potassium transport. The integument appears to play an active role in regulating the composition of the molting fluid, but its role in fluid transport remains to be determined.

Active Potassium Transport by the Isolated Lepidopteran Larval Midgut: Stimulation of Net Potassium Flux and Elimination of the Slower Phase Decline of the Short-Circuit Current

ABSTRACT Adenosine 3’:5’-cyclic monophosphate (cyclic AMP), Antibiotic A23187, caffeine, cholera toxin, dibutyryladenosine 3’ :5’-cyclic monophosphate (dbcAMP), 5-hydroxytryptamine (5-HT), larval blood, and theophylline were tested for their effects on active potassium transport, as measured by the short-circuit current (SCC), in isolated Manduca sexta larval midgut. None of the tested materials affected the short-circuit current during the rapid phase of its usual exponential decline, and only dbcAMP and larval blood affected the short-circuit current during the slower phase of its exponential decline. Dibutyryl-cyclic AMP stimulated an increase in short-circuit current and net potassium flux (measured using 42K). Both unidirectional potassium fluxes increased but there was no effect on the flux ratio or on the rate at which net potassium transport declined with time. A dialysable extract of fifth instar larval blood effected potassium transport in a manner similar to that of dbcAMP, indicating that larval blood contains natural transport-stimulating factors. A dialysable extract of fourth instar larval blood not only stimulated potassium transport but also prevented the slow phase of decline in the short-circuit current. Therefore, in addition to transport-stimulating factors present in fifth instar blood, fourth instar blood appears to contain substances which prevent degeneration of at least the transport related functions of midgut in vitro. It is argued that the action of the transport-stimulating factor in larval blood on the electrogenic cation pump in larval midgut cells is mediated by cyclic AMP without involving a change in intracellular calcium ion concentration.

Role of the medullary collecting duct in potassium excretion in potassium-adapted animals

Previous studies have demonstrated that the rate of urinary potassium excretion is markedly greater in animals fed a high potassium diet than in animals on a control diet before and during the acute infusion of potassium salts. Because the contribution of the medullary collecting duct to urinary potassium under these conditions has not been determined, microcatheterization studies were performed to elucidate the role of that nephron segment in regulating potassium excretion in controls and in animals on a potassium-enriched diet. Although there was no evidence of net transport of potassium by the medullary collecting duct in control animals under basal conditions, net secretion of potassium by that nephron segment accounted for nearly one half of the increased rate of urinary excretion in animals fed a high potassium diet. During acute infusion of potassium salts, potassium secretion by the medullary portion of the collecting duct contributed approximately one half of the potassium in the final urine samples in both controls and animals fed a high potassium diet. Because the rate of urinary excretion was twofold greater in experimental animals during acute potassium loading, absolute potassium secretion in medullary collecting duct was twice the control rate in animals adapted to a high potassium dietary intake. These data demonstrate, therefore, that the medullary collecting duct plays an important role in regulating the excretion of potassium when the excretory load is either acutely or chronically increased.

Luminal influences on potassium secretion: sodium concentration and fluid flow rate

Two methods of in vivo continuous microperfusion were used to evaluate separately luminal sodium concentration and fluid flow rate as factors regulating potassium secretion by the renal distal tubule of the rat. Emphasis was placed on evaluating changes in sodium concentration (43-97 mM) and flow rate (4-27 nl/min) within the physiological range. Absolute rates of Na, K, Cl, and H2O transport were measured. Results showed that increasing early distal flow rate without increasing early distal Na concentration significantly increased the absolute rate of potassium secretion by the distal tubule. In contrast, increasing early distal Na concentration, distal Na delivery, and distal Na absorption did not affect potassium secretion if flow rate was not changed. Further studies showed that reducing early distal Na concentration below the physiological range (to 15 mM) caused the direction of net sodium transport to be reversed but did not significantly reduce potassium secretion. Increasing early distal K concentration (to 34 mM) caused the direction of net potassium transport to be reversed. The rate of potassium secretion appears to depend in part on the luminal potassium concentration. Increases in luminal flow rate may increase the rate of potassium secretion by lowering the luminal K concentration.

Refinements in the short-circuit technique and its application to active potassium transport across the cecropia midgut.

1. The conventional, two-electrode method for measuring potential difference across an epithelium is subject to error due to potential gradients caused by current flow in the bathing medium. Mathematical analysis shows that the error in measuring short-circuit current is proportional to the resistivity of the bathing medium and to the separation of the two recording electrodes. It is particularly serious for the insect larval midgut, where the resistivity of the medium is high, and that of the tissue is low. 2. A system has been devised, which uses a third recording electrode to monitor directly the potential gradient in the bathing medium. By suitable electrical connexions, the gradient can be automatically compensated, leaving a residual error which depends on the thickness of the tissue, but not on the electrode separation. Because the thicknesses of most epithelia are smaller than the smallest practical electrode spacing, this error is smaller than that inherent in a two-electrode system. 3. Since voltage-gradients are automatically compensated, it is possible to obtain continuous readings of potential and current. A 'voltage-clamp' circuit is described, which allows the time-course of the short-circuit current to be studied. 4.The three-electrode system has been used to study the larval midgut of Hyalophora cecropia. The average results from five experiments were: initial potential difference (open-circuit): 98+/-11 mV (S.E.M.); short-circuit current at time 60 min: 498+/-160 microA cm=2; 'steady-state' resistance at 60 min: 150+/-26 omega cm2. The current is equivalent to a net potassium transport of 18.6 mu-equiv cm-2 h-1. 5. The electrical parameters of the midgut change rapidly with time. The potential difference decays with a half-time of about 158 min, the resistance increases with a half-time of about 16 min, and the short-circuit current decays as the sum of two exponential terms, with half-times of about 16 and 158 min respectively. In addition, potential and short-circuit current show transient responses to step changes. 6. The properties of the midgut are compared with those of other transporting epithelia, and their dependence on the degree of folding of the preparation is discussed. Their time-dependence is discussed in the context of changes in potassium content of the tissue, and the implications for measurements depending on the assumption of a steady state are outlined.

Collecting duct function in deoxycorticosterone acetate-escaped, normal, and salt-deprived rats. Response to hypervolemia.

The microcatheterization technique was used to study reabsorption of fluid, sodium, and potassium in the medullary collecting duct in chronically deoxycorticosterone acetate (DOCA)-treated and salt-loaded rats, as well as in normal and chronically salt-deprived (NaD) rats, before and after infusion of donor blood (33% of estimated circulating volume). Before expansion, urinary sodium excretion was highest in DOCA rats, intermediate in normal, and lowest in low salt rats. Significant collecting duct reabsorption was found in NaD, normal, and DOCA groups. In contrast to sodium, no net transport of potassium was found in any series. During intravascular expansion, increased renal excretion of fluid and sodium was observed uniformly in both DOCA and normal groups, whereas a diuretic response was found in five of seven rats, and a natriuretic response in four of seven rats of the NaD group. Natriuresis of DOCA rats was significantly greater than that of either normal or responding NaD rats. Diuresis and natriuresis in all three series were assocaited with complete inhibition of fluid and sodium reabsorption from the lumen of the medullary collecting duct, whereas such reabsorption persisted in nonresponding low salt rats. Increased sodium excretion in DOCA rats in comparison to the other two series could be explained by enhanced intratubular delivery of the ion to the medullary collecting system. I conclude that the renal response to acute blood volume expansion is due primarily to complete inhibition of both fluid and sodium reabsorption in the medullary collecting duct, but that differences in tubular delivery may modify the resulting diuresis and natriuresis.

Renal control of intestinal sodium and water transport in the dog.

The influence of an intravenous infusion of saline on the absorption of water and sodium by the jejunum has been investigated in dogs previously submitted to sodium-rich or poor diets. While the net intestinal transport was reduced in sodium-loaded animals, no response was observed in the sodium-deprived dogs, despite identical changes in arterial pressure, intravascular volume and blood dilution indexes. The intestinal response of sodium-deprived dogs became positive after transplanting to their neck vessels the kidneys removed from sodium-loaded animals, thus demonstrating that the presence in the blood of a humoral message of renal origin is required to permit the inhibition of net transport. The difference of the responses depended on the variations of the mucosa-to-serosa unidirectional flux. The net potassium transport did not change significantly. The experimental conditions made unlikely an interference of mineralocorticosteroids, angiotensin or antidiuretic hormone. The present results suggest that the kidney might modulate sodium transport in the jejunum, and perhaps elsewhere in the body, by the way of an additional endocrine function.

Effects of Cholecystokinin and Metoclopramide on Jejunal Movements of Water and Electrolytes and on Transit Time of Luminal Fluid in Man

Abstract. The effects of cholecystokinin and metoclopramide upon jejunal transit time of luminal fluid, net movements of water and electrolytes and unidirectional fluxes of sodium were studied in 11 normal subjects, each one being his own control. An intestinal perfusion technique with a four‐lumen tube was used. This allowed a simultaneous determination of mean transit time and absorption rate of water and electrolytes through a 35 cm segment of jejunum, (a) Cholecystokinin induced a significant decrease in mean transit time of fluid along the test segment. This effect was primarily due to a striking reduction (40% or more) in the mean diameter of the intestinal lumen, (b) Simultaneously there was a significant increase in net water, sodium and chloride secretion into the lumen, whereas net transport of potassium and bicarbonate was not affected. The lumen‐to‐blood unidirectional flux of sodium was obviously reduced but the opposite flux did not significantly change, (c) Similar changes in water and electrolyte movements were observed in subjects in whom transit time was primarily decreased by metoclopramide. (d) A close correlation was found between changes in transit time and net water and sodium transport into the lumen, in both cholecystokinin and metoclopramide studies.These results suggest that intestinal hypermotility may result, per se, in an increased secretion rate of water and electrolytes across the proximal small bowel. The implication of these findings in clinical conditions associating watery diarrhoea with intestinal hypermotility is discussed.

Net potassium transport in neurospora: Properties of a transport mutant

Net K + uptake by wild-type Neurospora shows a complex dependence on the extracellular pH. From pH 4 to 6, uptake follows standard Michaelis Menten kinetics as a function of external potassium but shifts to sigmoid kinetics at pH 8. Net flux measurements have now been carried out on mutant strain R2449, isolated by virtue of an abnormally high potassium requirement for growth, and previously shown to have an elevated K 1 2 for steady-state K + exchange at pH 5.8. The results indicate that R2449 is abnormal in net K + uptake at pH 4, 5.8 and 8, consistent with the notion that a single cation transport system exists in Neurospora, capable of functioning over the entire pH range. Two models are presented, an allosteric model and a 2-site model, which can account quantitatively for the shift from Michaelis-Menten kinetics at low pH to sigmoid kinetics at high pH and for the defect in R2449. Further experiments will be needed to distinguish between the models.

Steady-state concentrations of potassium in the ocular fluids

The steady-state concentrations of potassium in the plasma, aqueous humours and vitreous body of the rabbit, cat and dog have been measured. The results show that the fluids are by no means in equilibrium with the plasma in respect to this ion, and the relative concentrations in anterior and posterior aqueous humours, and the anterior and posterior halves of the vitreous body, may best be explained on the assumption of the secretion of a high-potassium fluid by the ciliary epithelium associated with passive diffusion across the iris and choroid. In addition, the active accumulation of potassium by the anterior surface of the lens, associated with passive diffusion from the posterior surface, may modify the relative concentrations in aqueous humours and vitreous body. Studies on the effect of incubation of the isolated eye demonstrate the existence of a net transport of potassium from aqueous humour to vitreous body by way of the lens. The effects of raising the plasma concentration of potassium on the concentrations of this ion in the ocular fluids suggest that the influx by way of the ciliary body is controlled by an active, or carrier, transport process that is saturated at normal plasma concentrations. By infusion of RbCl, a competitive inhibition of the influx of potassium into the posterior aqueous humour may be demonstrated. It is concluded that it is unlikely that the pigment epithelium of the retina is concerned with active transport of potassium into the vitreous body.