Membrane Of Frog Skin Research Articles

Evidence for P2Y-type ATP receptors on the serosal membrane of frog skin epithelium.

The present study presents the first evidence for P2Y-type adenosine 5'-triphosphate (ATP) receptors on the basolateral membranes of frog skin epithelial cells. Cytosolic calcium ([Ca2+]i) was measured with fura-2 and Calcium-Green-1 using epifluorescence microscopy and confocal laser scanning microscopy respectively. In the presence of Ca2+ in the solutions ATP increased [Ca2+]i. The increase in [Ca2+]i was due to the agonist activity of ATP and not to the activity of the potential products of ATP metabolism, i.e. adenosine 5'-diphosphate (ADP), adenosine 5'-monophosphate (AMP) or adenosine, as shown by a comparison of the magnitude of the increases in [Ca2+]i caused by the various compounds. The rise in [Ca2+]i was predominantly monophasic at low ATP concentrations (below 100 microM). At higher concentrations the initial spike was followed by a plateau phase. In the absence of Ca2+ in the extracellular solution ATP caused Ca2+ release from intracellular stores. This could be inhibited by pre-treatment of the tissue with 1 microM thapsigargin, an inhibitor of the endoplasmic reticulum calcium ATPase. The nucleotide uridine 5'-triphosphate (UTP) had similar effects on [Ca2+]i although the plateau level of the [Ca2+]i response was higher with this P2Y agonist. Confocal laser scanning microscopy showed that all cell layers of the epithelium responded to ATP. Our data indicates that serosal ATP acts on serosal P2Y-type receptors in frog skin epithelium. This is the first evidence of a phospholipase C-coupled receptor in this tissue.

Ca(2+)-blockable, poorly selective cation channels in the apical membrane of amphibian epithelia. UO2(2+) reveals two channel types.

This study deals with the effect of mucosal UO2(2+) on the Ca(2+)-blockable, poorly selective cation channels in the apical membrane of frog skin and toad urinary bladder. Our data show that UO2(2+) inhibits the Na+ currents through the amiloride-insensitive cation pathway and confirm a previously described stimulatory effect on the amiloride-blockade Na+ transport. Noise analysis of the Ca(2+)-blockable current demonstrates that the divalent also depresses the low-frequency Lorentzian (fc = 11.7 Hz) in the power density spectrum (PDS) and reveals the presence of high-frequency relaxation noise (fc = 58.5 Hz). The action of UO2(2+) is not reversed upon washout and is not accompanied by noise, typically induced by reversible blockers. The divalent merely depresses the plateau of the low-frequency Lorentzian, demonstrating a decrease in the number of conductive cation channels. Similarly, with mucosal K+ and Rb+, UO2(2+) also unmasks the high-frequency Lorentzian by depressing the noise from the slowly fluctuating cation channels (type S). In all experiments with mucosal Cs+, the PDS contains high-frequency relaxation noise (fc = 75.1 Hz in Rana temporaria, and 65.4 Hz in Rana ridibunda). An effect of UO2(2+) on the Cs+ currents and Lorentzian plateaus could not be demonstrated, suggesting that this monovalent cation does not pass through type S channels. Experiments with the urinary bladder revealed only a UO2(2+)-insensitive pathway permeable for Na+, K+, Rb+, and Cs+. We submit that in frog skin two cation-selective channels occur, distinguished by their spontaneous gating kinetics, their sensitivity to UO2(2+), and their permeability for Cs+. In toad urinary bladder, only one kind of cation-selective channel is observed, which resembles the UO2(2+)-insensitive channel in frog skin, with fast open-closed kinetics (type F).

Poorly selective cation channels in apical membranes of epithelia.

The apical membrane of frog skin contains two types of pathways which allow the passage of several monovalent cations in the absence of external Ca2+. Differences between the two pathways concern their open-close kinetics, selectivity, and the affinity for several blocking agents. Type S channels open and close relatively slowly, whereas type F channels display fast open-close kinetics. Both channel types allow the passage of Na+, K+, and Rb+ currents which are blocked by divalent cations and La3+ added to the extracellular side. Type F channels are permeable for Cs+ which is, however, excluded from type S channels. Shifts in open-close kinetics induced by Mg2+ occur at concentrations below 5 microM for type F channels, whereas more than a tenfold higher dose is required for the type S pathway. UO2(2+) concentrations up to 100 microM only occlude type S channels while 100 microM tetracaine selectively blocks type F channels. Apical membranes of toad urinary bladder, cultured amphibian renal epithelia (A6), and toad colon contain only type F channels. In toad bladder and A6 cells volume expansion strongly activates this pathway. Macroscopic currents carried by Ba2+ and Ca2+ could be recorded after activation of toad bladders with oxytocin and treatment of the apical surface with nanomolar concentrations of Ag+, which seems to interact with a site located at the channel interior.

Blockage of Na+ currents through poorly selective cation channels in the apical membrane of frog skin and toad urinary bladder.

The blockage of Na+ movements through the poorly selective cation channels in the apical membrane of frog skin (Rana temporaria) and toad urinary bladder (Bufo marinus) was investigated with noise, impedance analysis and microelectrode techniques. Na+ currents through this pathway were studied with NaCl Ringer solutions on both sides. After removal of Ca2+ and other divalent cations from the mucosal compartment, a considerable part of Isc became insensitive to amiloride. In frog skin, the inhibitory effect of amiloride in mucosal Ca(2+)-free solutions was highly variable. In some experiments a complete lack of inhibition was observed. Similarly, in the absence of amiloride, the inhibitory effect of mucosal Ca2+ varied strongly among frogs. In the absence of mucosal Ca2+, analysis of the fluctuation in Isc revealed a Lorentzian component in the power density spectrum. The corner frequency (fc) of this spontaneous Lorentzian was 12.3 Hz in frog skin and 347 Hz in the toad urinary bladder. In frog skin, nanomolar concentrations of mucosal Ca2+ induced an additional Lorentzian noise component. Its corner frequency shifted upwards with increasing mucosal Ca2+ concentration ([Ca2+]m). The relation between 2 pi fc and [Ca2+]m was linear at small [Ca2+]m whereas a parabolic increase of fc was observed at the highest [Ca2+]m. In the bladder, nanomolar concentrations of mucosal Ca2+ did not induce an additional noise component but modified the spontaneous Lorentzian noise by increasing fc proportionally with [Ca2+]m. Microelectrode recordings demonstrated that at least part of the Ca(2+)-blockable current passes through the granulosum cells and confirmed the apical localization of the poorly selective cation channel. The lack of the inhibitory effect of amiloride in Ca(2+)-free solutions seems to originate from the parallel arrangement of the amiloride- and Ca(2+)-blockable pathways and from influences of the blockage of apical channels on the basolateral membrane conductances. The latter cross-talk seems to find its origin in the voltage dependence of the basolateral membrane conductance [Garty H (1984) J Membr Biol 77:213-222; Nagel W (1985) Pflügers Arch 405 [Suppl 1]:S39-S43].

Current-voltage relations of Cs+-inhibited K+ currents through the apical membrane of frog skin.

The voltage-dependence of the inhibitory effect of mucosal Cs+ on the inward K+ current through the apical membrane of frog skin (Rana temporaria) was studied by recording transepithelial current-voltage relations. Experiments were performed with skins exposed to NaCl and KCl Ringer solutions on the serosal and mucosal side respectively (control skins), as well as with tissues incubated with K2SO4 Ringer solutions on both sides (depolarized skins). Studies of the dose-dependence of the Cs+ block showed that under both experimental conditions the apparent affinity of Cs+ increased as the transepithelial potential was clamped at higher mucosal positive voltages. Under control conditions, the concentration of Cs+ required to block 50% of the K+ current (KCs) recorded while the transepithelial voltage was clamped at zero mV was 16 mmol/l. KCs decreased exponentially with mucosal positive voltages. The dependence of KCs on the membrane potential was analyzed with Eyring rate theory in which Cs+ was assumed to block the K+ transport by binding to a site within the channel. The analysis showed that this site is located at a relative electrical distance delta = 0.32 of the voltage drop across the apical membrane, measured from the cytosolic side. The Hill coefficient obtained from this analysis was n = 3.1. Experiments with K+-depolarized tissues showed that only inward K+ currents recorded with positive transepithelial voltages were depressed by external Cs+. Also under these conditions KCs showed an exponential dependence on the transepithelial potential. The analysis of these data with the rate theory revealed delta = 0.09 and n = 1.7.(ABSTRACT TRUNCATED AT 250 WORDS)

Voltage-dependent Ba2+ block of K+ channels in apical membrane of frog skin

The characteristics of the blockage of apical K+ channels in the frog skin (Rana temporaria) by Ba2+ were investigated with current-voltage measurements and current-fluctuation analysis. Inward K+ currents were recorded with a transepithelial K+ concentration gradient oriented from mucosa to serosa. When Ba2+ (5-10,000 microM) was added to the mucosal solution, the inward K+ current was progressively depressed. This blockage was strongly voltage dependent. The apparent macroscopic Michaelis-Menten constant decreased exponentially with increasing transepithelial voltage (Vt) (mucosa positive). According to Eyring rate theory, the binding site for the Ba2+ ion in the K+ channel was found to be located at a relative electrical distance of 0.72 of the apical membrane potential field, measured from the cytosolic side. From current-voltage (I-V) measurements and Michaelis-Menten kinetics, the Ba2+ dissociation constant was calculated: KBa = 57 microM (Vt = 0 mV). The voltage dependence of the on- and off-rate of the Ba2+-receptor interaction was obtained from the analysis of current fluctuations induced by Ba2+. An exponential relationship between the rates and Vt was obtained, as was found for KBa from the I-V measurements. KBa (at Vt = 0 mV) calculated from the noise experiments was 66 microM.

Effect of sodium on amiloride- and triamterene-induced current fluctuations in isolated frog skin.

The apparent association constants of two agents, amiloride and triamterene, that block the Na-selective channel of apical membrane of frog skin are shown to decrease as the Na concentration is increased in the apical bathing solution in isolated skin of the frog, Rana temporaria, Rana esculenta, and Rana pipiens. These results were obtained in "normally polarized" skins. These effects were independent of the anion used (chloride or methylsulfate) or the cation used as the Na substitute (Tris, DDA, or K ion). When NaCl was replaced with mannitol, the Na effect on the amiloride association rate constant persisted, which shows that ionic strength was not critically involved. The amiloride corner frequency was unaffected when the clamp potential was altered from +100 to -60 mV. The Na dependence was greatly attenuated or absent when the serosal surface was bathed in 120 mM K Ringer's, an effect that appears to be attributable to some pharmacological effect of high serosal K. A previously described three-state model is used to analyze the inhibitory effect of Na on the blocker association rate constant.

Autoregulation of apical membrane Na+ permeability of tight epithelia. Noise analysis with amiloride and CGS 4270.

Noise analysis of the Na+ channels of the apical membranes of frog skin bathed symmetrically in a Cl-HCO3 Ringer solution was done with amiloride and CGS 4270. Tissues were studied in their control states and after inhibition of transepithelial Na+ transport (Isc) by addition of quinine or quinidine to the apical solution. A critical examination of the amiloride-induced noise indicated that the single channel Na+ currents (iNa) were decreased by quinine and quinidine, probably because of depolarization of apical membrane voltage. Despite considerable statistical uncertainty in the methods of estimation of the Na+ channel density with amiloride-induced noise (NA, see text), the striking observation was a large increase of NA with amiloride inhibition of the rate of Na+ entry into the cells. NA was increased to 406% of control, whereas Isc was inhibited to 8.6% of control by 6 microM amiloride. Studies were done also with the Na+ channel blocker CGS 4270. Noise analysis with this compound was advantageous, permitting iCGSNa and NCGS to be measured in individual tissues with a relatively small inhibition of Isc. As with amiloride, inhibition of Isc with CGS 4270 caused large increases of the Na+ channel density (approximately 200% at approximately 35% inhibition of the Isc). Quinine and quinidine caused an approximately 50% increase of Na+ channel density while inhibiting iNa by approximately 60-70%. As inhibition of Na+ entry leads to an increase of Na+ channel density, a mechanism of autoregulation appears to be a major factor in adjusting the apical membrane Na+ permeability of the cells.

Physiological role of apical potassium ion channels in frog skin.

The K+ permeability of the apical membrane of frog skin (Rana temporaria) was analysed by recording the short-circuit current and its fluctuations in the presence of a mucosa-to-serosa-oriented K+ concentration gradient. Loading of the animals with KCl resulted in an augmentation of the Ba2+-blockade component of the short-circuit current and the plateau value of the K+-dependent relaxation noise. Poisoning of active transport and exposing both sides of the epithelium to KCl Ringer solution caused an increase of the K+ current and its fluctuations recorded after restoring the inward-oriented K+ gradient. Serosal quinidine (5 X 10(-4) M), which is thought to increase intracellular Ca2+ activity, depressed the K+ current and the relaxation noise. This effect was completely reversible. Removal of Na+ from the serosal solution, which is known to result in an elevation of intracellular Ca2+ by abolishing the driving force for the Na+/Ca2+ exchanger, also reduced the K+ current and the Lorentzian plateau. Both parameters returned to their control values after restoring the Na+ gradient across the basolateral membranes. It is concluded from these experiments that the apical K+ permeability is controlled by factors which depend on the intracellular K+ and Ca2+ concentration and that the apical K+ channels may constitute a pathway for K+ secretion.

Noise analysis of inward and outward Na+ currents across the apical border of ouabain-treated frog skin

The passive Na+ transport across the apical membrane of frog skin (Rana catesbeiana) was studied under the following circumstances: (1) control conditions (sulfate Ringer's, K+ depolarised serosal membranes); (2) after blocking the active transport step with ouabain; (3) with an outward oriented Na+ current. The amiloride-induced Na+ current fluctuations were analysed to calculate the density of amiloride blockable channels and the current through one single channel. Despite the large reduction of the macroscopic current by ouabain, the single channel current remained unchanged, while the number of amiloride blockable Na+ channels was reduced by a factor of eight. It is concluded from these observations that the earlier described reduction of the permeability of the apical membrane is caused by a decrease of the number of electrically conductive Na+ channels. The outward oriented single channel currents were less than 50% of the currents in the opposite direction. After ouabain, the number of Na+ channels was independent from the current direction.

Permeability studies on animal membrane/carbohydrate systems

Hydrodynamic permeability measurements on water, and on aqueous solutions of d-glucose and sucrose of various concentrations, through frog-skin membrane were made. The conductance of the membrane equilibrated with the permeants was also measured. Some comments regarding the dependence of the permeability coefficient and the membrane conductance on the concentration were made. It was observed that the membrane behaves anisotropically in so far as the hydrodynamic permeability is concerned.

Apical K+ channels in frog skin (Rana temporaria): cation adsorption and voltage influence gating kinetics.

Open-close kinetics of fluctuating K+ channels in the apical frog skin membrane were studied with noise analysis of the K+ current (IK). The mucosa to serosa directed IK was obtained with serosal NaCl- and mucosal KCl-Ringer under voltage clamp conditions. Mucosal protons (pH greater than 4), several polyvalent metal ions, and choline shifted the plateaus (SO) of the Lorentzian component in the IK noise spectrum to higher, but the corner frequency (fc) to lower values. SO was lowered at pH less than 4, due to a K+-channel block by H+. Ca2+, Sr2+, H+ (pH greater than 4) and choline did not affect IK. A slight reduction of IK was seen with Mg2+, Mn2+, Co2+, Ni2+, Zn2+, Cu2+ and La3+. At pH greater than 4, the H+-induced shifts in SO an fc were almost abolished in solutions of high mucosal Ca2+ concentrations. Clamping the transepithelial potential difference to more positive values (with respect to the serosa) shifted the Lorentzian parameters SO and fc in the same way as the cations did. As with protons, mucosal Ca2+ interferred with the effect of voltage. The interference of cationic (probably fixed charge screening) and voltage effects suggests a common, more general mechanism of action, namely alterations in K+-channel fluctuation kinetics by changes in local electrical fields. On this basis, the rates for the open-close reaction of K+ channels and their mean lifetime were calculated. We found that e.g. increasing [Ca2+]O from 1-10 mM caused no change of the mean open time, but increased the mean time "closed" of the K+ channel by a factor of about 1.5. Other mucosal cations, as well as depolarizing clamp potentials are thought to have the same effect.

Time course of pump inhibition by ouabain in amphibian epithelia

Inhibition by ouabain of rheogenic Na + transport across the basolateral membranes of frog skin is found to be manifest within 3–4 min. This rate of pump inhibition is not different from the rate of diffusion through extracellular tissue layers between the serosal bath and the actual site of action, i.e., the epithelial cell layers. It is concluded that the well-known slow time course of decrease in transepithelial current flow is due ionic redistribution and conductance changes of the epithelial membranes secondary to pump inhibition.

Spontaneous fluctuations of potassium channels in the apical membrane of frog skin.

1. The previously demonstrated K+-dependent short-circuit current through the skin of frog species Rana temporaria (Zeiske & Van Driessche, 1979), bathed with mucosal K+- and serosal Na+-Ringer solution, was investigated with current-fluctuation analysis. 2. The current-noise spectra were recorded in the frequency range from 1 to 800 Hz and showed a Lorentzian component with a mean plateau value S0 = (1.50 +/- 0.05).10(-20) A2.s.cm-2 and a corner frequency of fc=(81.0 +/- 3.4)Hz(n=14). 3. S0 increased with mucosal K+ concentration, [K]o, while fc remained almost unchanged. A decrease in S0 was observed when serosal Na+ was replaced by K+. 4. Mucosal Cs+ (10 mM) depressed, reversibly, the K+-dependent current noise to the level of the background noise. Moreover, a linear decrease in fc with increasing Cs+ concentration was observed. 5. Among the other tested alkali cations, Rb+ was the only blocker though less potent than Cs+. Tetraethylammonium, 4-aminopyridine, 2.4.6-triaminopyrimidine and amiloride had no effect. 6. Alterations in the transcellular transport of Na+ contained in a mucosal solution with high [K]o resulted in significant changes in K+ current noise. 7. The current-fluctuation intensities decreased with increasing contact time to high [K]o; these changes were concomitant with the previously reported time dependence of the short-circuit current (Zeiske & Van Driessche, 1979). 8. The K+-dependent fluctuations are thought to originate from K+-selective pathways in the apical cell membranes. The description of the K+-current noise by a single Lorentzian suggests that the "K+ channels" switch randomly between an open and closed state. 9. Assuming a two state model for the channel-kinetics, the single channel current i and the channel density M were calculated as i=(0.37 +/- 0.05)pA and M=(0.53 +/- 0.08) mu-2 (n=13).

Effect of ouabain on electrical conductance of frog skin. Evidence against recycling of sodium

Ouabain (10 −4 M) added to the serosal solution of isolated frog skin not only stops the active transport of Na + but causes a dramatic increase in the electric conductance of the skin. The effect also appears when ouabain is added to amiloride-pretreated skins, ruling out the possibility of a cellular effect. The similarity between the effect of ouabain on normal and amiloride-pretreated skins indicates that no appreciable recycling of Na + across the basolateral membrane of frog skin takes place. The change of Na + efflux after ouabain is added to amiloride-pretreated skins parallels the change of electric conductance, indicating that besides blocking the Na + pump, ouabain affects the paracellular shunt pathway between the cells.

Ba2+-Induced conductance fluctuations of spontaneously fluctuating K+ channels in the apical membrane of frog skin (Rana temporaria)

We studied the influence of mucosal Ba2+ ions on the recently described (Zeiske & Van Driessche, 1979a, J. Membrane Biol. 47:77) transepithelial, mucosa towards serosa directed K+ transport in the skin of Rana temporaria. The transport parameters G (conductance), PD (potential difference), Isc (short-circuit current, "K+ current"), as well as the noise of Isc were recorded. Addition of millimolar concentrations of Ba/+ to the mucosal K+-containing solution resulted in a sudden but quickly reversible drop in Isc. G and Isc decreased continuously with increasing Ba2+ concentration, (Ba2+)o. The apparent Michaelis constant of the inhibition by Ba2+ lies within the range 40-80 microM. The apical membrane seems to remain permselective for K+ up to 500 microM (Ba2+)o. Higher (Ba2+)o, however, appears to induce a shunt (PD falls, G increases). This finding made an accurate determination of the nature of the inhibition difficult but our results tend to suggest a K+-channel block by K+-Ba2+ competition. In the presence of Ba2+, the power spectrum of the K+ current shows a second Lorentzian component in the low-frequency range, in addition to the high-frequency Lorentzian caused by spontaneous K+-channel fluctuations (Van Driessche & Zeiske, 1980). Both Lorentzian components are only present with mucosal K+ and can be depressed by addition of Cs+ ions, thus indicating that Ba2+ ions induce K+-channel fluctuations. The dependence of the parameters of the induced Lorentzian on (Ba2+)o shows arise in the plateau values to a maximum around 60 microM (Ba2+)o, followed by a sharp and progressive decrease to very low values. The corner frequency which reflects the rate of the Ba2+-induced fluctuations, however, increases quasi-linearly up to 1 mM (Ba2+)o with a tendency to saturate at higher (Ba2+)o. Based on a three-state model for the K+ channel (having one open state, one closed by the spontaneous fluctuation and one blocked by Ba2+) computer calculations compared favorably with our results. The effect of Ba2+ could be explained by assuming reversible binding at the outer side of the apical K+ channel, thereby blocking the open channel in ;competition with K+. The association-dissociation of Ba2+ at its receptor site is thought to cause a chopping of the K+ current, resulting in modulated current fluctuations.

Does intracellular sodium regulate sodium transport across the mucosal surface of frog skin?

A method has been devised to functionally remove the serosal membrane of frog skin. Skins treated in this way have no spontaneous potential. However, if sodium gradients are placed across the tissues diffusion potentials and hence short-circuit currents of either sign, depending on the direction of the gradient, could be recorded. These short-circuit currents were completely inhibited by amiloride only from the mucosal face. However, the concentration of amiloride causing 50% inhibition of the short-circuit current ( K m ) in treated skins was 2.3 · 10 −3 M, when a sodium gradient was applied from serosa to mucosa, whereas both in untreated skins without a sodium gradient and in treated skins with a mucosal to serosal sodium gradient, the K m of amiloride was 2·10 −7-4·10 −7 M. The mechanism by which amiloride is able to inhibit the short-circuit currents of either sign is discussed.

Effects of antidiuretic hormone upon electrical potential and resistance of apical and basolateral membranes of frog skin

The effect of ADH upon the intracellular potential and the resistance of inner and outer borders of the transport pathway was investigated on isolated skins of Rana temporaria. Within 40 min after ADH (100--300 mU/ml), the intracellular potential under short-circuit conditions decreased to about 40% of the control value (--79 +/- 4 mV), concomitant with an increase in the short-circuit current to about 160% of the control value. Amiloride, applied when steady values under ADH had been reached, caused an immediate rise of the intracellular potential to values typical for control conditions. This confirms (i) the intracellular location of the microelectrode and the absence of impalement artifacts, and (ii) the ineffectiveness of ADH upon the electromotive forces of the inner border. ADH had no effect upon the intracellular potential after blockage of the Na entry by Amiloride. The equilibrium potential of the outer border was estimated to be about +20mV under the influence of ADH. As this value is considerably less positive than might be expected for the chemical potential of Na, a significant contribution of ions other than Na to the outer border conductance and equilibrium potential is implicated. The resistance of the outer border was more significantly decreased than that of the active transcellular pathway after ADH due to an increase in the inner border resistance, which exceeded that of the outer border after ADH. The effect of ADH upon the outer membrane characteristics would be underestimated by a factor of two, if the alterations of the electrical potential difference were not taken into consideration.

The stimulation of Na + uptake in frog skin by uranyl ions

1. 1. The Na + uptake in the isolated frog skin of Rana esculenta was measured by the short-circuit current ( I sc). Uranyl ions increase at pH 5.5 the I sc up to 200% at concentrations of 10 mM. The half-maximal value for this effect is at about 1 mM uranyl salt. 2. 2. The effect is (a) specific for the Na +-transporting pathways in the outer Na +-selective membrane, (b) fully reversible. No stimulation can be seen in presence of 1 mM H + or 0.1 mM amiloride. 3. 3. The decrease of the sodium permeability of the apical membrane ( P Na), normally induced by increasing concentrations of Na + in the mucosal solution, [Na] 0, is partially prevented by uranyl ions. The apparent Michaelis constant of the saturable Na + uptake is shifted to much higher values. 4. 4. A comparison between the uranyl effect and similar effects of other drugs leads to the conclusion that uranyl ions might act in a polar hydrophobic environment, possibly by combining with phosphate groups (of phospholipids), and, thus, enhancing Na + permeability by changes in tertiary structure near each Na channel. The interaction of mucosal Na + with their receptor, normally triggering the [Na] 0-dependent decrease of P Na, is thought to be diminished by uranyl association in a neighbouring region, causing a non-competitive stimulation of the Na + translocation through the apical frog skin membrane.

A factor in pre-eclamptic serum affecting sodium transport across a membrane.

SummaryThe serum from non‐pregnant and normotensive pregnant women and from women with pre‐eclampsia tested for its effect on the rate of sodium transport across a frogskin membrane. There is a factor in pre‐eclamptic serum which alters the rate of sodium transport.