Transport In Toad Urinary Bladder Research Articles

Cell Cl and transepithelial Na transport in toad urinary bladder

Relationships between short-circuit current (Isc), cell Cl and the mechanism(s) of Cl accumulation in toad bladder epithelial cells were investigated. In serosal Cl-free gluconate Ringer, 80% of the cell Cl (measured by x-ray microanalysis) was lost over 30-60 min with an associated decrease in cell water content. concomitantly, Isc fell to 20% of its initial value within 10 min but then recovered to 45% of its initial value despite continued Cl loss. With the reintroduction of Cl, cell Cl and Isc both recovered within 10 min. Serosal SITS (4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonate; 0.5 mM) plus bumetanide (0.1 mM), did not prevent the fall in Isc or the loss of cell Cl in gluconate medium, although they did inhibit subsequent recovery of Isc in this medium. They also prevented the recovery of Isc in Cl medium but not the reaccumulation of Cl by the cells. Although SITS and bumetanide did not prevent the loss or recovery of Cl, they modified the pattern of the ion changes. In their absence, changes in cellular Cl were twice that of the changes in measured cellular cations implicating basolateral Cl/HCO3 exchange in Cl movement. With SITS plus bumetanide present, changes of similar magnitude in Cl were associated with equivalent changes in cation, consistent with the inhibition of Cl/HCO3 exchange.

Role of PKC isozymes in water transport in toad urinary bladder

Protein kinase C (PKC) isozymes, when activated, are translocated to particulate membrane fractions for transport to the apical membrane surface in a variety of cell types. Evidence of PKC translocation was demonstrated in human megakaryoblastic leukemic cells, and in cardiac myocytes and fibroblasts, using FTTC immunofluorescent antibody labeling techniques. Recently, we reported immunogold localizations of PKC subtypes I and II in toad urinary bladder epithelia, following 60 min stimulation with Mezerein (MZ), a PKC activator, or antidiuretic hormone (ADH). Localization of isozyme subtypes I and n was carried out in separate grids using specific monoclonal antibodies with subsequent labeling with 20nm protein A-gold probes. Each PKC subtype was found to be distributed singularly and in discrete isolated patches in the cytosol as well as in the apical membrane domains. To determine if the PKC isozymes co-localized within the cell, a double immunogold labeling technique using single grids was utilized.

Cholera toxin enhances adenylate cyclase-dependent transport in toad urinary bladder

Cholera toxin (CT) irreversibly ADP-ribosylates and activates the nucleotide-stimulatory (Ns) subunit of adenylate cyclase in many tissues, thereby eliciting cyclase-dependent functions. Although earlier studies performed at room temperature could not demonstrate CT-stimulated water transport in toad urinary bladder, subsequent work in other tissues has emphasized the need for incubation at 35-37 degrees C to effect ribosylation and the subsequent physiological effects. We found that incubating tissues with amphibian culture media, rather than Ringer solution, maintained tissue viability at this higher temperature and permitted prolonged incubation with CT. At 37 degrees C, in the presence of 0.1 mM phosphodiesterase inhibitor (1-methyl-3-isobutylxanthine, MIX), 0.2-200 nM mucosal CT caused a dose-dependent but submaximal enhancement of water flux and urea transport. Elimination of MIX from the bath diminished subsequent CT-induced stimulation, supporting a role for adenosine 3',5'-cyclic monophosphate (cAMP) as mediator of the CT effect. The increased water flow was stable for greater than 1 h after removal of CT from the bath, consistent with irreversible stimulation of the cyclase. Mucosal CT stimulated transport to a greater degree than serosal CT, paralleling the pattern seen in the intestine, which is compatible with passage of the toxin's a subunit across the cell to the serosal membrane cyclase. Exposure of the tissue's mucosal surface to GM1 ganglioside, (the natural receptor for the CT b subunit) yielded maximal stimulation of water flow and near-maximal urea transport, presumably by increasing CT's binding to the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin-stimulated sodium transport in toad urinary bladder

Mammalian and teleost insulins increase active sodium transport by the toad urinary bladder at subnanomolar concentrations. This stimulation is evident within 15 min and persists for hours. Porcine proinsulin and a cross-linked derivative of bovine insulin are less effective than porcine insulin in stimulating the short-circuit current (SCC), indicating the specificity appropriate for activation of sodium transport through an insulin receptor. The initial stimulation by insulin of the SCC is not blocked by pretreatment with actinomycin D, puromycin, cycloheximide, or tunicamycin. However, in the presence of any one of these inhibitors the sustained increase in SCC is blocked and the rise is short-lived, lasting only 45 to 90 min. In amphotericin-treated bladders, the addition of insulin did not further stimulate SCC.

Possible role of Ca2+‐binding sites in the regulation of Na+ transport in toad urinary bladder

La3+ was used to assess the role of membrane-bound Ca2+ in the regulation of basal and antidiuretic hormone (ADH)-induced Na+ transport by the isolated toad urinary bladder. Na+ transport was monitored by means of a short-circuit current (Isc) device. Mucosal La3+ (0.5-5 mM) increased Isc, while serosal La3+ (5 mM) produced a biphasic response (stimulation followed by inhibition). The stimulatory effects of La3+ were additive when present on both sides and were suppressed by mucosal amiloride or serosal ouabain. The action of mucosal La+ was reversible but the inhibition produced by serosal La3+ was not. In the presence of serosal La3+ the natriferic effect of ADH was abolished, but Theophylline, dibutyryl-cAMP, Amphotericin B, mucosal La3+, mucosal low pH, and phospho(enol) pyruvate, were able to increase Isc. These results suggest that Ca2+ binding sites in apical and basolateral membranes may play a key role in the modulation of both basal and ADH-induced Na+ transport. Serosal La3+ apparently inactivates the hormone-receptor interaction and/or the link between the ADH-receptor complex and the activation of adenylate cyclase, but does not interfere with the operation of the Na+ "pump", the basal activity of adenylate cyclase or any of the intracellular events that mediate the effect of ADH on Na+ transport.

Thyroid hormone: Aldosterone antagonism in cultured epithelial cells

Thyroid hormone (T 3) has been demonstrated to inhibit the action of aldosterone on sodium transport in toad urinary bladder and rat kidney. We have exammined the effect of T 3 on aldosterone action and specific nuclear binding in cultured epithelial cells derived from toad urinary bladder. In cell line TB6-C, addition of 5·10 −8 M T 3 to culture media for up to 3 days results in no change in short-circuit current or transepithelial resistance. This concentration of T 3 completely inhibits the maximal increase in short-circuit current in response to 1·10 −7 M aldosterone. The inhibition can be demonstrated with 18 h preincubation or with simultaneous addition of T 3 and aldosterone. The half-maximal concentration for the inhibition of the aldosterone effect is approx. 5·10 −9 M T 3. T 3 has no effect on cyclic AMP-stimulated short-circuit current in these cells. The effect of T 3 on nuclear binding of [ 3H]aldosterone was examined using a filtration assay with data analysis by at least-squares curve-fitting program. Best fit was obtained with a model for two binding sites. The dissociation constants for the binding were K′ d1 = (0.82 ± 0.36)·10 −10 M and K′ d2 = (3.2±0.60)·10 −8 M.The half-maximal concentration for aldosterone-stimulated sodium transport in these cells is approx. 1·10 −8 M. Analysis of nuclear aldosterone binding in cells preincubated for 18 h with 5·10 −8 M T 3 showed a K′ d1 = (0.15 ± 0.10)·10 −10 M and K′ d2 = (3.5 ± 0.10)·10 −8 M. We conclude that T 3 i action of aldosterone on sodium transport at a site after receptor binding in the nucleus.

Effects of Adriamycin on Calcium and Water Transport in Toad Urinary Bladdera

Effects of Adriamycin on Calcium and Water Transport in Toad Urinary Bladder^a

Possible role of cytosolic calcium and Na-Ca exchange in regulation of transepithelial sodium transport

Emerging evidence in a number of different epithelia suggests that changes in cytosolic calcium ion levels play a critical role in the regulation of transepithelial sodium transport. Maneuvers believed to raise cytosolic calcium ion activity lead to an inhibition of net sodium transport in toad urinary bladder, frog skin, and isolated perfused proximal renal tubules. Regulation of the level of ionized calcium in the cytosol of the epithelial cells appears to involve a process of coupled Na-Ca exchange across the basolateral plasma membrane, energized, at least in part, by the sodium gradient. It is suggested that changes in cytosolic calcium ion levels, secondary to changes in Na-Ca exchange, in turn dependent in part on the activity of the sodium pump, constitute a link in a negative feedback mechanism. Through such a feedback mechanism, the rate of entry of sodium into the cell across the apical surface may be kept in step with its rate of extrusion across the basolateral surface.

PH-Dependence of water and solute transport in toad urinary bladder

Stimulation of urea and water transport by vasopressin (ADH) appears to occur via independent pathways. We examined the effects of altering serosal or mucosal bath pH on transport of water, urea, and sodium. Compared to bladders with a serosal bath pH of 7.4 to 8.0, reducing the serosal bath pH to 6.8 led to a 60% fall in ADH-stimulated osmotic water flow, without decreasing the permeability of urea. Raising the serosal pH to 9.5 had the opposite effect: urea permeability was inhibited by 40% without altering water flow. Exogenous cyclic AMP-stimulated water and urea permeabilities were not dissociated, but were changed in the same direction by alterations in serosal pH: serosal acidification enhanced the effect of exogenous cyclic AMP on both urea and water, whereas the cyclic AMP effect on both was diminished by serosal alkalinization. This was especially marked for urea, suggesting that an alteration in the urea response to cyclic AMP may be particularly important in defining vasopressin-stimulated urea permeability as the serosal bath pH is altered. Mucosal acidification increased short circuit current but decreased both the urea and water response to ADH and 8-bromo-cyclic AMP. The response to cyclic AMP was less consistent. Mucosal alkalinization did not cause significant changes in either basal or stimulated transport. The data demonstrate distinct and separable effects of bath pH alterations on each of the transport systems examined.

Effects of electrochemical gradients on active sodium transport in toad urinary bladder.

To determine the concentration dependence of active sodium transport in toad urinary bladder, bidirectional fluxes of sodium were measured at three mucosal sodium concentrations (Cm) (114, 27, and 3 mM), before and after addition of sufficient ouabain to eliminate active transport. The results permit estimation of E, the electromotive force of the sodium pump, and its conductance, ga. E averaged 137 mV and was unaffected by depolarization or by reduction of Cm; ga fell by only 40%, suggesting that a Cm of 3 mM was still above the half-maximal value for the sodium pump. However, net open-circuit transport was estimated to become zero at Cm = 6 mM, owing to backflux through the shunt path, which did not vary with Cm. The flux ratio in the active path exhibited the type of abnormality first described as "single-file pore diffusion," which is attributed to relatively tight coupling between transport and metabolism.

Energetics of sodium transport in toad urinary bladder.

The ratio of the rate of transepithelial sodium transport, JNa, across the isolated toad urinary bladder to the simultaneously measured rate of transport-dependent metabolism, JsbCO2, has been measured as a function of the transepithelial electrical voltage, deltapsi. The ratio remains constant with a mean value of 18 to 20 over the range of imposed voltages of 0 to +70 mV. With increasing hyperpolarization of the bladder, JNa decreases and the calculated electromotive force or apparent "ENa" of the sodium pump increases. From thermodynamic and kinetic arguments it is shown that the apparent "ENa" approaches the maximal electrochemical potential gradient, ENa, against which sodium can be transported by this tissue only when JNa approximately 0. At this unique condition F ENa (in which F is the Faraday constant) is the maximal free energy of the chemical reaction driving sodium transport and thus equal to the maximal extramitochondrial phosphorylation potential and the maximal free energy of the mitochondrial respiratory chain within the transporting cells.

Effect of magnesium on sodium transport in toad urinary bladder

Voltage-clamp techniques were employed to examine the effect of magnesium (Mg) on sodium transport in the isolated urinary bladder of the Dominican toad. Substitution of 1 mM Mg had no effect, but 3-mM Mg substitution resulted in a reversible increase in short-circuit current (27%) and potential difference (19%) and decrease in transepithelial resistance (14%); no greater effect was seen with 5- or 10-mM Mg substitution. The effect was produced by mucosal or mucosal and serosal Mg substitution; serosal Mg substitution was without effect. Analysis of electrical parameters disclosed that magnesium increased net sodium transport via an effect on the sodium pump.

Metabolic cost of sodium transport in toad urinary bladder

The metabolic cost of active sodium transport was determined in toad bladder at different gradients of transepithelial potential. Deltapsi, by continuous and simultaneous measurements of CO2 production and of transepithelial electric current. Amiloride was used to block active sodium transport in order to assess the nontransport-linked, basal, production of CO2 and the passive permeability of the tissue. From these determinations active sodium transport, Jna, and suprabasal CO2 production, Jsb CO2, were calculated. Since large transients in Jna and Jsb CO2 frequently accompanied any abrupt change in deltapsi, steady state conditions were carefully defined. Some 20 to 40 min were required after a change in deltapsi before steady state of transport activity and of CO2 production were achieved. The metabolic cost of sodium transport proved to be the same whether the bladder expended energy moving sodium against a transepithelial electrical potential grandient of +50 mV or whether sodium was being pulled through "the active transport pathway" by an electrical gradient of -50 mV. In both cases the value of the ratio Jna/Jsb CO2 averaged some 20 sodium ions transported per molecule of CO2 produced. When the Na pump was blocked by 10(-2) M ouabain, the perturbations of the transepithelial electrical potential did not elicit changes of Jna nor, consequently of Jsb CO2. The independence of the ratio Jna/Jsb CO2 from deltapsi over the range+/-50 mV indicates a high degree of coupling between active sodium transport and metabolism.

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. II. Effects of different medium potassium concentrations on epithelial cell composition.

Epithelial cells from hemibladders incubated in potassium-free sodium Ringer's serosal medium lost potassium, both in exchange for serosal sodium and with chloride and water. Cellular sodium of mucosal origin did not change. The loss of cellular potassium, chloride and water closely followed the fall in short-circuit current (SCC). One third as much potassium, chloride and water were lost in 1 mM potassium serosal medium; SCC fell 1/3 as much. Potassium-free choline Ringer's serosal medium abolished the initial increase in SCC and reduced the fall in cellular potassiu, chloride and water and in SCC. Ouabain (10(-2)M) in potassium-free medium prevented the initial increase in SCC and the loss of cellular chloride and water. Ouabain (5 X 10(-4)M) caused loss of cellular potassium in exchange for mucosal and serosal sodium, effects different from those of absence of serosal potassium although SCC was similarly inhibited. Sodium-free mucosal medium abolished SCC and prevented the initial transient of SCC and diminished loss of cellular potassium, chloride and water on removing serosal potassium. When serosal potassium concentration was increased considerably, cells gained potassium, chloride and water, and in 116 mM potassium media, lost sodium of serosal origin. A hypothesis is advanced to explain the transients in SCC on changing serosal potassium concentration. The fall in cellular potassium, not water, probably inhibits sodium transport in media of less than 2 mM potassium.

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. I. Effects of different medium potassium concentrations on electrical parameters.

When serosal medium potassium was decreased from the usual concentration of 3.5 mM, the short-circuit current (SCC) of hemibladders in chambers immediately and transiently increased. The maximum SCC attained was greater the greater the decrease in serosal potassium, and was twice the initial SCC when the final serosal medium was potassium-free. The SCC then fell to its previous level for final serosal potassium concentrations greater than 2 mM and to less than its previous level for those less than 2 mM, being lowest (15% of previous levle) in potassium-free sodium Ringer's. When serosal medium potassium was increased from 3.5 mM by substituting potassium for sodium, SCC transiently decreased and then recovered to its previous level. Steady SCC was the same in serosal media of 2-116 mM potassium; conductance increased and p.d. decreased after incubation in 50-116 mM potassium serosal media. Short-circuit current and p.d. transiently increased (decreased) whenever serosal medium potassium was decreased (increased); conductance increased with any change in serosal potassium. Changing mucosal medium potassium concentration between 0 and 50 mM did not affect SCC. The initial transient increase and subsequent decrease in SCC on removing serosal potassium were partially prevented by 3.5 mM rubidium or caesium, or by 116 mM choline in the serosal medium. The transient changes in SCC were due partly to changes in transepithelial sodium transport.

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. III. Exchangeability of epithelial cellular potassium.

The exchangeability of toad bladder epithelial cell potassium has been investigated. An insignificant amount of cellular potassium exchanged with mucosal medium 42K. From the rate of uptake of 42K into the cells from the serosal medium at least two cellular potassium pools were identified. The more rapidly exchanging pool contained about one-quarter to one-third of the cellular potassium and exchanged with a half-time of about 30 min. It was from this pool that potassium was lost from cells exposed to ouabain or to a potassium-free medium. In addition, when 3.5 mM rubidium replaced 3.5 mM potassium in sodium Ringer's the epithelial cells lost in 60 min about one-quarter of their cellular potassium in exchange for rubidium. Inhibition of transepithelial sodium transport by amiloride, 10(-5) mM, seemed to depress the rate of potassium uptake into the more rapidly exchanging pool without affecting total cellular potassium content. However, stimulation of transepithelial sodium transport by vasopressin appeared not to affect the rate of potassium uptake. The rate of potassium uptake into this pool seemed much less than that required for a tight 1:1 coupling between transepithelial sodium transport and potassium uptake. The remaining cellular potassium exchanged at a much slower rate and even after 19 hours of incubation only 67% of cellular potassium was labelled. If this slower exchanging potassium represents a single pool, 99% of cellular potassium would be labelled only after incubation with 42K for 56 hours.

Effect of stretch on passive transport in toad urinary bladder.

In order to gain further information about the effect of stretch on the urinary bladder of the toad, transepithelial movement of radioactive sucrose, chloride, and urea was measured across bladder sacs during acute changes in the internal volume. Short-circuit current (SCC) and total tissue conductance (Kt) were also measured in each experiment. It was found that sudden large increases or smaller graded increases in volume resulted in a consistent fall in the tracer permeability (P*) of all three isotopes. However, this fall was due entirely to the larger area term in the calculation of P* rather than any real change in isotope movement. When total diffusion (TD) of each isotope was calculated by a method that eliminated the changes in surface area, it was apparent that stretch produced no significant effects on the transepithelial movement of any of these three molecules. Large stretch also resulted in parallel increases in SCC and Kt in most bladders. We conclude from these observations that the intercellular pathway for sucrose and chloride and the transcellular pathway for urea are unaltered by degrees of stretch that enhance SCC and sodium transport. By inference, the observed increases in Kt appear to represent changes in specific active pathway conductance (Ka), and may relate importantly to the changes in sodium transport.

Action of ouabain on sodium transport in toad urinary bladder, Evidence for two pathways for sodium entry.

The cardiac glycoside ouabain inhibits transepithelial sodium transport in the toad urinary bladder. It is shown that this drug reduces the rate coefficient for sodium exit at the serosal pump site. In addition, ouabain inhibits entry across the mucosal border whenever the electrochemical potential gradient for sodium is made less favorable. The data are interpreted as indicating the existence of two separate pathways for sodium entry, one of which is ouabain inhibitable.

Interrelationship of H+ excretion and Na+ reabsorption in the toad urinary bladder.

Recent results from this laboratory have shown that in the absence of mucosal Na+ and exogenous CO2, H+ excretion is reduced in the toad urinary bladder. This study was done to determine if H+ excretion is linked to Na+ reabsorption in the toad bladder. Na+ transport was inhibited by ouabain or by substitution of the sodium with choline chloride. Both of these agents produced an inhibition of H+ excretion. However, when dinitrophenol was added to stimulated CO2 production by the tissue, H+ excretion returned to control levels even though Na+ transport was still inhibited. Vasorressin, which stimulates Na+ transport in toad urinary bladder, had no effect on H+ excretion. In addition, simultaneous energies of activation were detemined for H+ excretion and Na+ reabsorption in the toad bladder. The activation energies for the two processes were significantly different. These results suggest that Na+ and H+ are not coupled in an exchange mechanism at the mucosal surface of the cell. H+ excretion, however, does appear to be limited by the endogenous CO2 production of the bladder in the absence of exogenous CO2.

Effects of anions on sodium transport in toad urinary bladder.

ARTICLESEffects of anions on sodium transport in toad urinary bladderI Singer, and MM CivanI Singer, and MM CivanPublished Online:01 Oct 1971https://doi.org/10.1152/ajplegacy.1971.221.4.1019MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited BySmooth muscle aldolase C-bound inositol 1,4,5-trisphosphate studied in vitro under physiological conditionsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, Vol. 1401, No. 1Enhancing Effects of Binary Mixtures of Acid With Salt on the Gustatory Neural Activity in the Clawed Toad, Xenopus laevisBrain Research Bulletin, Vol. 42, No. 5Ion and Water Transport in Toad Urinary Epithelia in Vitro1 January 2011Electrical transients produced by the toad bladder in response to altered serosal composition at constant osmolalityBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 1108, No. 1Transport-related modulation of the membrane properties of toad urinary bladder epitheliumBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 1070, No. 1Chapter 5 Sodium Dependence of Cation Permeabilities and TransportCatecholamine stimulation of ion transport in the toad urinary bladderBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 945, No. 1Apical Na+ permeability of frog skin during serosal Cl− replacementThe Journal of Membrane Biology, Vol. 102, No. 2Cellular Models of Epithelial Ion TransportCellular Models of Epithelial Ion TransportCell K activity in frog skin in the presence and absence of cell currentThe Journal of Membrane Biology, Vol. 85, No. 2Effects of anions on cellular volume and transepithelial Na+ transport across toad urinary bladderThe Journal of Membrane Biology, Vol. 83, No. 1-2Factors affecting the transport of β-amino acids in rat renal brush-border membrane vesicles. The role of external chlorideBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 812, No. 3Electrogenic transport of 5-oxoproline in rabbit renal brush-border membrane vesicles Effect of intravesicular potassiumBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 732, No. 1Sodium gradient-dependent L-glutamate transport in renal brush border membrane vesicles. Evidence for an electroneutral mechanism.Journal of Biological Chemistry, Vol. 255, No. 16Effect of external cation and anion substitutions on sodium transport in isolated frog skinThe Journal of Membrane Biology, Vol. 52, No. 2Effect of FeCl3 on ion transport in isolated frog skinThe Journal of Membrane Biology, Vol. 52, No. 2Chapter 21 Electrogenic and Electroneutral Na+ Gradient-Dependent Transport Systems in the Renal Brush Border Membrane VesicleThe stimulation of Na+ uptake in frog skin by uranyl ionsBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 509, No. 2The role of Cl− ions in the neurotransmitter and redox regulation of ion movements through isolated frog skinComparative Biochemistry and Physiology Part C: Comparative Pharmacology, Vol. 59, No. 2Relation between chloride exchange diffusion and a conductive chloride pathway across the isolated skin of the toad ( Bufo bufo )Acta Physiologica Scandinavica, Vol. 102, No. 1Mode of action of amiloride in toad urinary bladderThe Journal of Membrane Biology, Vol. 32, No. 1Effect of anions on amiloride-sensitive, active sodium transport across rabbit colon,in VitroThe Journal of Membrane Biology, Vol. 37, No. 1Transport in Membrane Vesicles Isolated from the Mammalian Kidney and IntestineA new model for regulation of sodium transport in high resistance epitheliaMedical Hypotheses, Vol. 2, No. 3Energetics of the Na+-dependent transport of D-glucose in renal brush border membrane vesicles.Journal of Biological Chemistry, Vol. 250, No. 22Inhibition of active sodium transport by radiographic contrast mediaKidney International, Vol. 7, No. 2Chloride transport in isolated skin of Rana esculentaPfl�gers Archiv European Journal of Physiology, Vol. 355, No. 2Chloride flux via a shunt pathway in frog skin: Apparent exchange diffusionBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 282 More from this issue > Volume 221Issue 4October 1971Pages 1019-1026 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.221.4.1019PubMed4999967History Published online 1 October 1971 Published in print 1 October 1971 Metrics