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PubMed1989

Impaired oxygenation of gastric mucosa in portal hypertension. The basis for increased susceptibility to injury.

Increased susceptibility to mucosal damage is a prominent feature of portal hypertensive gastropathy. Since the portal hypertensive gastric mucosa has extensive microvascular changes, we postulated that the increased sensitivity to mucosal damage could have an ischemic basis. We measured distribution of gastric serosal and mucosal oxygenation in a group of portal hypertensive and sham-operated rats, and then studied the effects of intragastric aspirin. In the basal state, gastric mucosa of portal hypertensive rats had significantly reduced oxygenation compared to controls (24 +/- 5 vs 45 +/- 7 mm Hg PO2, P less than 0.02), while serosal oxygenation was similar between the two groups. Intragastric aspirin produced significantly greater mucosal damage to portal hypertensive rats and mucosal oxygenation was almost one third that of sham-operated controls. Systemic arterial pressures and oxygenation were similar between the two groups. We conclude that there is impairment of gastric mucosal oxygenation and increased mucosal damage by aspirin in portal hypertensive rats compared with sham-operated controls. These results support our hypothesis that the increased sensitivity of the portal hypertensive mucosa to damage is a consequence of impaired mucosal oxygenation.

Animals↗
PubMed1975

Electrical properties of the cellular transepithelial pathway in Necturus gallbladder. I. Circuit analysis and steady-state effects of mucosal solution ionic substitutions.

Microelectrode techniques were employed to measure the electrical resistance of the cell membranes and the shunt pathway, and the equivalent electromotive forces (EMF's) at both cell borders in Necturus gallbladder epithelium. The cell is, on the average, 57 mV negative to the mucosal solution and 59 mV negative to the serosal solution. The transepithelial potential (Vms) ranges from 0.5 to 5 mV, serosal solution positive. Assuming that the shunt EMF (Vs) is zero with standard Ringer's bathing oth sides of the tissue, both cell membrane EMF's are oriented with the negative pole toward the cell interior and are 39.9 +/- 3.6 mV (apical, Va), and 69.4 +/- 1.8 mV (basal-lateral, Vb)...

Animals↗
PubMed1982

Active and passive Na+ fluxes across the basolateral membrane of rabbit urinary bladder.

The apical membrane of rabbit urinary bladder can be functionally removed by application of nystatin at high concentration if the mucosal surface of the tissue is bathed in a saline which mimics intracellular ion concentrations. Under these conditions, the tissue is as far as the movement of univalent ions no more than a sheet of basolateral membrane with some tight junctional membrane in parallel. In this manner the Na+ concentration at the inner surface of the basolateral membrane can be varied by altering the concentration in the mucosal bulk solution. When this was done both mucosal-to-serosal 22Na flux and net change in basolateral current were measured. The flux and the current could be further divided into the components of each that were either blocked by ouabain or insensitive to ouabain. Ouabain-insensitive mucosal-to-serosal Na+ flux was a linear function of mucosal Na+ concentration. Ouabain-sensitive Na+ flux and ouabain-sensitive, Na+-induced current both display a saturating relationship which cannot be accounted for by the presence of unstirred layers. If the interaction of Na+ with the basolateral transport process is assumed to involve the interaction of some number of Na+ ions, n, with a maximal flux, MMAX, then the data can be fit by assuming 3.2 equivalent sites for interaction and a value for MMAX of 287.8 pM cm-2 sec-1 with an intracellular Na concentration of 2.0 mM Na+ at half-maximal saturation. By comparing these values with the ouabain-sensitive, Na+-induced current, we calculate a Na+ to K+ coupling ratio of 1.40 +/- 0.07 for the transport process.

Animals↗
PubMed1976

Amide transport channels across toad urinary bladder.

Urea and other small amides cross the toad urinary bladder by a vasopressinsensitive pathway which is independent of osmotic water flow. Amide transport has characteristics of facilitated transport: saturation, mutual inhibition between amides, and selective depression by agents such as phloretin. The present studies were designed to distinguish among several types of transport including (1) movement through a fixed selective membrane channel and (2) movement via a mobile carrier. The former would be characterized by co-transport (acceleration of labeled amide flow in the direction of net flow of unlabeled amide), the latter by counter-transport (acceleration of labeled amide flow in the opposite direction). Mucosal to serosal (M leads to S) and serosal to mucosal (S leads to M) permeabilities of labeled amides were determined in paired bladders. Unlabeled methylurea, a particularly potent inhibitor of amide movement, was added to either the M or S bath, while osmotic water flow was eliminated by addition of ethylene glycol and ethanol could not be demonstrated. Methylurea did not alter water permeability or transmembrane electrical resistance. The demonstration of co-transport is consistent with the presence of ADH-sensitive amide-selective channels rather than a mobile carrier.

Acetamides↗
PubMed1976

Differential covalent labeling of apical and basal-lateral membranes of the epithelium of the toad bladder.

The apical (luminal) plasma membrane of toad bladder epithelial cells has been labeled with (125I) diazo-diiodo sulfanilic acid (125I-DDISA) as demonstrated by electron-microscopic autoradiography. The silver grains (125I) were localized exclusively to the apical surface. At concentrations of DDISA of 10(-3) M or less, binding to the apical membrane had no significant effect on the fine structure of the epithelium. At concentrations of DDISA of 10(-6) M or less, the baseline short-circuit current (SCC), and the response to cyclic 3',5'-adenosine monophosphate (cAMP) plus theophylline were unimpaired. At 10(-5) M, baseline SCC was unchanged and the response to cyclic AMP plus theophylline was enhanced. At concentrations of 10(-4) M and greater baseline SCC was depressed and the response to the nucleotide inhibited. The basal-lateral epithelial plasma membranes were labeled by exposing the serosal side to pyridoxal phosphate and reducing the resultant Schiff base with sodium borotritide (3H-NaBH1). In electron-microscopic autoradiographs, the silver grains (3H) were found over the basal and lateral surfaces of the epithelium. At concentrations of pyridoxal phosphate of 10(-4) M and 3H-NaBH1 of 10(-3) M, there were no significant changes in the fine structure of the epithelium. Addition of pyridoxal phosphate (10(-4) M) and NaBH4 (10(-3) M) to the serosal side decreased the baseline SCC significantly but not the response to vasopressin. Covalent attachment of the 125I and the 3H was indicated by resistance to elution in the preparation of the sections for electron-microscopy and the reagent requirements for binding.

Animals↗
PubMed1984

Apical membrane area of rabbit urinary bladder increases by fusion of intracellular vesicles: an electrophysiological study.

Mammalian urinary bladder undergoes, in a 24-hour period, a series of slow fillings and rapid emptying. In part the bladder epithelium accommodates volume increase by stretching the cells so as to eliminate microscopic folds. In this paper we present evidence that once the cells have achieved a smooth apical surface, further cell stretching causes an insertion of cytoplasmic vesicles resulting in an even greater apical surface area per cell and an enhanced storage capacity for the bladder. Vesicle insertion was stimulated by application of a hydrostatic pressure gradient which caused the epithelium to bow into the serosal solution. Using capacitance as a direct and nondestructive measure of area we found that stretching caused a 22% increase in area. Removal of the stretch caused area to return to within 8% of control. An alternate method for vesicle insertion was swelling the cells by reducing mucosal and serosal osmolarity. This perturbation resulted in a 74% increase in area over a 70-min period. Returning to control solutions caused area to decrease as a single exponential with an 11-min time constant. A microtubule blocking agent (colchicine) did not inhibit the capacitance increase induced by hypoosmotic solutions, but did cause an increase in capacitance in the absence of a decreased osmolarity. Microfilament disrupting agent (cytochalasin B, C.B.) inhibited any significant change in capacitance after osmotic challenge. Treatment of bladders during swelling with C.B. and subsequent return to control solutions increased the time constant of the recovery to control values (22 min). The Na+-transporting ability of the vesicles was determined and found to be greater than that of the apical membrane. Aldosterone increased the transport ability of the vesicles. We conclude that some constituent of urine causes a loss of apical membrane permeability. Using electrophysiological methods we estimated that the area of cytoplasmic vesicles is some 3.3 times that of the apical membrane area. We discuss these results in a general model for vesicle translocation in mammalian urinary bladder.

Animals↗
PubMed1980

Relationship of transient electrical properties to active sodium transport by toad urinary bladder.

Application of voltage pulses of 10 mV for periods of 9 sec across toad urinary bladder elicits a rapid deflection in transepithelial current. Frequently, the current decays back towards its baseline value during the course of the polarizing pulse. This transient phenomenon can be induced, or its magnitude increased, by raising the mucosal or serosal Na+ concentration. The transient can be abolished by sufficiently hyperpolarizing the tissue (rendering serosa positive to mucosa), by inhibiting transcellular Na+ transport with amiloride or ouabain, and by increasing the serosal K+ concentration. Vasopressin increases net Na+ movement across toad bladder but does not elicit these transients. It is proposed as a working hypothesis for further study that the transient behavior characterized in this study reflects: (1) the partition of Na+ between the apical plasma membrane and contiguous fluid layers, (2) the partition of K+ between the basolateral plasma membrane and adjacent submucosal fluid layer, and (3) the negative feedback interaction between intracellular Na+ activity and Na+ permeability of the apical plasma membrane of the transporting cells.

Amiloride↗
PubMed1986

The volume of mitochondria-rich cells of frog skin epithelium.

The pathway for movement of chloride ions across frog skin is not well understood. Mitochondria-rich (MR) cells have been proposed as the route for chloride across the skin. To test this hypothesis we studied the MR cells of the skin of the frog, Rana pipiens, by quantitative light microscopic determination of cell volume. MR cell volume was influenced by changes in the chloride concentration or osmolality of the outside bathing solution. MR cells shrank about 23% when all chloride was removed from the outside (mucosal) bathing solution. MR cells were also shown to be responsive to changes in the osmolality of either the mucosal or serosal bath. Osmotically-induced swelling caused by dilution of the serosal bath resulted in volume regulatory decrease. These results are consistent with the hypothesis that MR cells constitute the pathway for chloride movement across frog skin.

Animals↗
PubMed1979

Saturable K+ pathway across the outer border of frog skin (rana temporaria): kinetics and inhibition by Cs+ and other cations.

The reaction of abdominal skins of the frog species Rana temporaria on mucosal K+-containing solutions was studied in an Ussing-type chamber by recording transepithelial potential difference (PD), short-circuit current (SCC) and conductance (G). With Na-Ringer's as serosal medium, a linear correlation between PD and the logarithm of the mucosal K+-concentration ([K]o) was obtained. The K+-dependent SCC saturated with increasing [K]o, and could quickly and reversibly be depressed by addition of Rb+, Cs+, and H+. Li+, Na+, and NH4+ did not influence K+ current. A large scatter was obtained for kinetic parameters like the slope of the PD-log[K]o-line (18--36.5 mV/decade), the apparent Michaelis constant (13--200 mM), and the maximal current of the saturable SCC (6--50 microa . cm-2), as well as for the degree of inhibition by Cs+ ions. This seemed to be caused by a time-dependent change during long time exposure to high [K]o (more than 30 sec), thereby inducing a selectivity loss of K+-transporting structures, together with an increase in SCC and G and a decrease in PD. Short time exposure to K+-containing solutions showed a competitive inhibition of K+ current by Cs+ ions, and a Michaelis constant of 6.6 mM for the inhibitory action of Cs+. Proton titration resulted in a decrease of K+ current at pH less than 3. An acidic membrane component (apparent dissociation constant 2.5 x 10(-3) M) is virtually controlling K+ transfer. Reducing the transepithelial K+-concentration gradient by raising the serosal potassium concentration was accompanied by the disappearance of SCC and PD.

Animals↗
PubMed1979

Electrical properties of the cellular transepithelial pathway in Necturus gallbladder: III. Ionic permeability of the basolateral cell membrane.

The ionic permeability of the basolateral membrane of Necturus gallbladder epithelium was studied with intracellular microelectrode techniques. After removal of most of the subepithelial tissue (to reduce unstirred layer thickness), impalements were performed from the serosal side, and ionic substitutions were made in the serosal solution while a microelectrode was kept in a cell. Thus, it was possible to obtain continuous (and reversible) records of transepithelial and cell membrane potentials and to measure intermittently the transepithelial resistance and the ratio of cell membrane resistances. From these data and the mean value of the equivalent resistance of the cell membranes in parallel (obtained from cable analysis in a different group of tissues), absolute cell membrane and shunt resistances and equivalent electromotive forces (emfs) were calculated. From the changes of basolateral membrane emf (Eb) produced by the substitutions, the conductance (G) and permeability (P) of the membrane for K, Cl and Na were estimated. Potassium-for-sodium substitutions produced large reductions of both cell membrane potentials, of Eb, and of the resistance of the basolateral membrane (Rb), indicating high GK and PK. Chloride substitution with isethionate or sulfate resulted in smaller changes of cell membrane potentials and Eb and in no significant change of Rb, indicating small but measurable values of GCl and PCl. Sodium substitutions with N-methyl-D-glucamine (NMDG) resulted in cell potential changes entirely attributable to the biionic potential produced in the shunt pathway (PNa greater than PNMDG), and in no significant changes of Rb or Eb, indicating that GNa and PNa are undetectable. The question of the mechanism of Cl transport across the basolateral membrane was addressed by comparing the mean rate of transepithelial Cl transport : formula, see text: and the predicted passive Cl flux across the basolateral membrane (from the membrane Cl conductance, potential, and Cl equilibrium potential). The conclusion is that only a very small fraction of the Cl flux across the basolateral membrane can be electrodiffusional. Since the paracellular Cl conductance is also too low to account for : formula, see text:, these results suggest the presence of a neutral mechanism of Cl extrusion from the cells. This could be a NaCl pump, a downhill KCl transport mechanism, or a Cl-HCO3 exchange mechanism.

Animals↗
PubMed1987

Cell membrane water permeability of rabbit cortical collecting duct.

The water permeability (Posm) of the cell membranes of isolated perfused rabbit cortical collecting ducts was measured by quantitative light microscopy. Water permeability of the basolateral membrane, corrected for surface area, was 66 microns X sec-1 for principal cells and 62.3 microns X sec-1 for intercalated cells. Apical membrane Posm values corrected for surface area, were 19.2 and 25 microns X sec-1 for principal and intercalated cells, respectively, in the absence of antidiuretic hormone (ADH). Principal and intercalated cells both responded to ADH by increasing Posm of their apical membranes to 92.2 and 86.2 microns X sec-1, respectively. The ratio of the total basolateral cell membrane osmotic water permeability to that of the apical cell membrane was approximately 27:1 in the absence of ADH and approximately 7:1 in the presence of the hormone for both cell types. This asymmetry in water permeability is most likely due to the fact that basolateral membrane surface area is at least 7 to 8 times greater than that of the apical membrane. Both cell types exhibited volume regulatory decrease when exposed to dilute serosal bathing solutions. Upon exposure to a hyperosmotic serosal bath (390 mosM), principal cells did not volume regulate while two physiologically distinct groups of intercalated cells were observed. One group of intercalated cells failed to volume regulate; the second group showed almost complete volume regulatory increase behavior.

Animals↗
PubMed1980

Influence of extracellular Cl concentration on Cl transport across isolated skin or Rana pipiens.

The effect of changes in Cl concentration in the external and/or serosal bath on Cl transport across short-circuited frog skin was studied by measurements of transepithelial Cl influx (J13Cl) and efflux (J31Cl), short-circuit current, transepithelial potential, and conductance (Gm). J14Cl as well as J31Cl were found to have a saturating component and a component which is apparently linear with Cl concentration. The linear component of J31Cl appears only upon addition of Cl to external medium, and about 3/4 of this component does not contribute to Gm. The saturating component of J31Cl is only 5% of total J31Cl with 115mM Cl in the serosal medium. Replacement of 115 mM Cl- in external medium by SO4=, NO3-, HCO3- or I- results in 87-97% reduction of J31Cl, whereas replacement with Br- has no effect. As external Cl concentration is raised in steps from 2 to 115 mM, J13Cl and J31Cl increase by the same amount but J13Cl is persistently 0.15 mueg/cm2hr larger than J31Cl. These results indicate that at least 3/4 of linear components of J13Cl and J31Cl proceed via an exchange diffusion mechanism which seems to be located at the outer cell border. The saturating component of J13Cl is involved in active Cl transport in an inward direction, and there is evidence suggesting that Cl uptake across outer cell border, which proceeds against an electrochemical gradient, is electroneutral but not directly linked to Na.

Animals↗
PubMed1986

Apical membrane K conductance in the toad urinary bladder.

The conductance of the apical membrane of the toad urinary bladder was studied under voltage-clamp conditions at hyperpolarizing potentials (mucosa negative to serosa). The serosal medium contained high KCl concentrations to reduce the voltage and electrical resistance across the basal-lateral membrane, and the mucosal solution was Na free, or contained amiloride, to eliminate the conductance of the apical Na channels. As the mucosal potential (Vm) was made more negative the slope conductance of the epithelium increased, reaching a maximum at Vm = -100 mV. This rectifying conductance activated with a time constant of 2 msec when Vm was changed abruptly from 0 to -100 mV, and remained elevated for at least 10 min, although some decrease of current was observed. Returning Vm to +100 mV deactivated the conductance within 1 msec. Ion substitution experiments showed that the rectified current was carried mostly by cations moving from cell to mucosa. Measurement of K flux showed that the current could be accounted for by net movement of K across the apical membrane, implying a voltage-dependent conductance to K (GK). Mucosal addition of the K channel blockers TEA and Cs had no effect on GK, while 29 mM Ba diminished it slightly. Mucosal Mg (29 mM) also reduced GK, while Ca (29 mM) stimulated it. GK was blocked by lowering the mucosal pH with an apparent pKI of 4.5. Quinidine (0.5 mM in the serosal bath) reduced GK by 80%. GK was stimulated by ADH (20 mU/ml), 8-Br-cAMP (1 mM), carbachol (100 microM), aldosterone (5 X 10(-7) M for 18 hr), intracellular Li and extracellular CO2.

Animals↗
PubMed1977

Electrical properties and active solute transport in rat small intestine. II. Conductive properties of transepithelial routes.

The transepithelial resistance, the cell membrane resistance and the ratio of resistances of the serosal (baso-lateral) to the mucosal (brush border) cell membrane were measured in rat duodenum, jejunum and ileum by means of microelectrode techniques. These measured values were not affected in the presence of actively transported solutes in the mucosal bathing fluid. Contribution of an electrical conductance through the extracellular shunt pathway to the total transepithelial conductance was quantitatively estimated using an electrically equivalent circuit analysis. These values estimated in respective tissues of small intestine were approx. 95% of the total transepithelial conductance, remaining unaffected by an active solute transport. From these data, the changes in emf's of the mucosal and serosal membrane induced by D-glucose or glycine were separately evaluated.

Animals↗
PubMed1980

Passive sodium movements across the opercular epithelium: the paracellular shunt pathway and ionic conductance.

The unidirectional Na+, Cl-, and urea fluxes across isolated opercular epithelia from seawater-adapted Fundulus heteroclitus were measured under different experimental conditions. The mean Na+, Cl0, and urea permeabilities were 9.30 x 10(-6) cm . sec-1, 1.24 x 10(-6) cm . sec-1, and 5.05 x 10(-7) cm . sec-1, respectively. The responses of the unidirectional Na+ fluxes and the Cl- influx (mucosa to serosa) to voltage clamping were characteristic of passively moving ions traversing only one rate-limiting barrier. The Na+ conductance varied linearly with, and comprised and mean 54% of, the total tissue ionic conductance. The Cl- influx and the urea fluxes were independent of the tissue conductance. Triaminopyrimidine (TAP) reduced the Na+ fluxes and tissue conductance over 70%, while having no effect on the Cl- influx of urea fluxes. Mucosal Na+ substitution reduced the Na+ permeability 60% and the tissue conductance 76%, but had no effect on the Cl- influx or the urea fluxes. Both the Na+ and Cl- influxes were unaffected by respective serosal substitutions, indicating the lack of any Na+/Na+ and Cl-/Cl- exchange diffusion. The results suggest that the unidirectional Na+ fluxes are simple passive fluxes proceeding extracelluarly (i.e., movement through a cation-selective paracellular shunt). This pathway is dependent on mucosal (external) Na+, independent of serosal (internal) Na+, and may be distinct from the transepithelial Cl- and urea pathways.U

Adaptation, Physiological↗
PubMed1976

Na+ transport by rabbit urinary bladder, a tight epithelium.

By in vitro experiments on rabbit bladder, we reassessed the traditional view that mammalian urinary bladder lacks ion transport mechanisms. Since the ratio of actual-to-nominal membrane area in folded epithelia is variable and hard to estimate, we normalized membrane properties to apical membrane capacitance rather than to nominal area (probably 1 muF approximately 1 cm2 actual area). A new mounting technique that virtually eliminates edge damage yielded resistances up to 78,000 omega muF for rabbit bladder, and resistances for amphibian skin and bladder much higher than those usually reported. This technique made it possible to observe a transport-related conductance pathway, and a close correlation between transepithelial conductance (G) and short-circuit current (Isc) in these tight epithelia. G and Isc were increased by mucosal (Na+) [Isc approximately 0 when (Na+) approximately 0], aldosterone, serosal (HCO-3) and high mucosal (H+); were decreased by amiloride, mucosal (Ca++), ouabain, metabolic inhibitors and serosal (H+); and were unaffected by (Cl-) and little affected by antidiuretic hormone (ADH). Physiological variation in the rabbits' dietary Na+ intake caused variations in bladder G and Isc similar to those caused by the expected in vivo changes in aldosterone levels. The relation between G and Isc was the same whether defined by diet changes, natural variation among individual rabbits, or most of the above agents. A method was developed for separately resolving conductances of junctions, basolateral cell membrane, and apical cell membrane from this G--Isc relation. Net Na+ flux equalled Isc. Net Cl- flux was zero on short circuit and equalled only 25% of net Na+ flux in open circuit. Bladder membrane fragments contained a Na+-K+-activated, ouabain-inhibited ATPase. The physiological significance of Na+ absorption against steep gradients in rabbit bladder may be to maintain kidney-generated ion gradients during bladder storage of urine, especially when the animal is Na+-depleted.

Adenosine Triphosphatases↗
PubMed1980

Influence of extracellular Cl concentration on Cl transport across isolated skin of Rana pipiens.

The effect of changes in Cl concentration in the external and/or serosal bath on Cl transport across short-circuited frog skin was studied by measurements of transepithelial Cl influx (JCl13) and efflux (JCl31), short-circuit current, transepithelial potential, and conductance (Gm). JCl13 as well as JCl31 were found to have a saturating component and a component which is apparently linear with Cl concentration. The linear component of JCl31 appears only upon addition of Cl to external medium, and about 3/4 of this component does not contribute to Gm. The saturating component of JCl31 is only 5% of total JCl31 with 115 mM Cl in the serosal medium. Replacement of 115 mM Cl- in external medium by SO4=, NO3-, HCO-3 or I- results in 87-97% reduction of JCl31, whereas replacement with Br- has no effect. As external Cl concentration is raised in steps from 2 to 115 mM, JCl13 and JCl31 increase by the same amount but JCl13 is persistently 0.15 mu eq/cm2hr larger than JCl31. These results indicate that at least 3/4 of linear components of JCl13 and JCl31 proceed via an exchange diffusion mechanism which seems to be located at the outer cell border. The saturating component of JCl13 is involved in active Cl transport in an inward direction, and there is evidence suggesting that Cl uptake across outer cell border, which proceeds against an electrochemical gradient, is electroneutral but not directly linked to Na.

Animals↗
PubMed1982

Noise analysis reveals K+ channel conductance fluctuations in the apical membrane of rabbit colon.

In this paper we describe current fluctuations in the mammalian epithelium, rabbit descending colon. Pieces of isolated colon epithelium bathed in Na+ or K+ Ringer's solutions were studied under short-circuit conditions with the current noise spectra recorded over the range of 1-200 Hz. When the epithelium was bathed on both sides with Na+ Ringer's solution (the mucosal solution contained 50 microM amiloride), no Lorentzian components were found in the power spectrum. After imposition of a potassium gradient across the epithelium by replacement of the mucosal solution by K+ Ringer's (containing 50 microM amiloride), a Lorentzian component appeared with an average corner frequency, fc = 15.6 +/- 0.91 Hz and a mean plateau value So = (7.04 +/- 2.94) x 10(-20) A2 sec/cm2. The Lorentzian component was enhanced by voltage clamping the colon in a direction favorable for K+ entry across the apical membrane. Elimination of the K+ gradient by bathing the colon on both sides with K+ Ringer's solutions abolished the noise signal. The Lorentzian component was also depressed by mucosal addition of Cs+ or tetraethylammonium (TEA) and by serosal addition of Ba2+. The one-sided action of these K+ channel blockers suggests a cellular location for the fluctuating channels. Addition of nystatin to the mucosal solution abolished the Lorentzian component. Serosal nystatin did not affect the Lorentzian noise. This finding indicates an apical membrane location for the fluctuating channels. The data were similar in some respects to K+ channel fluctuations recorded from the apical membranes of amphibian epithelia such as the frog skin and toad gallbladder. The results are relevant to recent reports concerning transcellular potassium secretion in the colon and indicate that the colon possesses spontaneously fluctuating potassium channels in its apical membranes in parallel to the Na+ transport pathway.

Animals↗