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PubMed1985

Effects of mucosal sodium removal on cell volume in Necturus gallbladder epithelium.

Necturus gallbladder epithelium transports sodium and chloride by a process that first involves the cellular entry of each ion across the apical membrane in an electrically silent process. In this paper we present results from cell volume and fluid flux measurements in the presence of different inhibitors and at normal and reduced sodium concentrations, which bear on the process by which ionic entry is effected. We find that reduction of mucosal sodium to a concentration of 10 mM has no effect on either cell volume or on the rate of transepithelial fluid transport, whereas the complete removal of sodium causes a significant decrease in cell volume in addition to its known inhibitory effect on fluid transport. Amiloride had no effect on cell volume at normal sodium concentrations but markedly reduced it when the sodium concentration was reduced to 10 mM. Amiloride, bumetanide, and dipyridamole markedly and reversibly inhibited fluid transport. Finally, the addition of ouabain to the serosal medium induced cell swelling, which was prevented by the removal of potassium from the mucosal medium. These results indicate that the process of sodium entry at the apical membrane is complicated and likely includes both cotransport (NaCl or Na-K-2Cl) and parallel exchange (Na-H and Cl-HCO3) transport mechanisms, and that the proportion of NaCl transported by the different mechanisms varies with the conditions.

Amiloride↗
PubMed1985

Microelectrode measurements from oxyntic cells in intact Necturus gastric mucosa.

The electrical properties of oxyntic cells were measured in intact isolated Necturus fundic mucosa by dissecting away the serosal muscle and connective tissue and impaling the oxyntic cells across their basolateral membranes. Their properties under resting [i.e., not secreting acid (10(-4) M serosal cimetidine)] and stimulated (10(-4) M histamine) conditions were compared with those of surface cells impaled across their apical membranes in a separate set of experiments. Histamine hyperpolarized the transepithelial potential by 6-10 mV and reduced the transepithelial resistance by approximately 40%. The basolateral membrane potential (Vcs) of both cell types was significantly hyperpolarized by histamine, that of oxyntic cells from a resting value of -50 to -59 mV (P less than 0.001) and that of surface cells from -50 to -54 mV (P less than 0.05). Histamine also hyperpolarized the apical membrane potential (Vmc) of the oxyntic cells; however, the Vmc of surface cells was significantly depolarized. The ratio of the apical to basolateral cell membrane resistances Ra/Rb (delta Vmc/delta Vcs resulting from transepithelial current pulses) of resting oxyntic cells was 1.1 and that of surface cells was 3.6. Stimulation did not affect the Ra/Rb of either cell type. A tenfold increase in serosal K+ concentration depolarized Vcs and increased Ra/Rb of resting and stimulated oxyntic cells, indicating a significant basolateral K+ conductance. The results are consistent with a purely passive role for surface cells and indicate that stimulation results in a simultaneous decrease of both the apical and basolateral membrane resistances of the oxyntic cells.

Animals↗
PubMed1987

Measurement of intracellular Ca2+ activity in Necturus gallbladder.

To clarify the effects of Ca2+-free solutions on the electrophysiological properties of leaky epithelia, Necturus gallbladder was mounted in an Ussing-type chamber and its mucosal surface exposed to Ca2+-free EGTA (2 mM) Ringer. Lateral-space width was controlled by a -3-cmH2O pressure gradient on the serosal outflow. Transepithelial potential difference and resistance were monitored while cell membrane potential and intracellular Ca2+ activity (Ca2+i) were determined with conventional and Ca2+-sensitive microelectrodes. Ca2+i averaged 183 +/- 27 nM (n = 15). Reduction of mucosal Ca2+ activity to approximately 500 nM reversibly lowered transepithelial resistance while cell membrane potential remained unaltered and fractional membrane resistance increased from 0.77 +/- 0.01 to 0.83 +/- 0.02 (P less than 0.01, n = 5). In five gallbladders mucosal Ca2+ reduction induced a significant drop in Ca2+i from 133 +/- 26 to 77 +/- 20 nM (P less than 0.01, n = 5) while transepithelial resistance fell from 125 +/- 27 to 107 +/- 24 omega X cm2 (P less than 0.01). These results indicate that transepithelial resistance decrements observed during exposure to Ca2+-free solutions stem from a reversible increase in tight-junctional but not cell membrane permeability and that this effect is associated with a fall in intracellular Ca2+ activity.

Animals↗
PubMed1988

Potassium-induced cell swelling in Necturus gallbladder epithelium.

In Necturus gallbladder epithelium, elevation of mucosal K+ to 95 mM in the presence of 10 mM Na+ resulted in cell swelling at a rate of 3.2% original volume per minute, followed by volume-regulatory shrinking. When Na+ was completely removed from or when amiloride (10(-4) M) was added to the mucosal medium, K+-induced cell swelling was abolished. In the presence of 10 mM Na+, 1 mM Ba2+ abolished and substitution of mucosal Cl- by NO-3 had no effect on K+-induced swelling. Thus solute entry following elevation of mucosal K+ is effected by separate K+ and Cl- pathways. Furthermore, substitution of 95 mM K+ for Na+ in the mucosal bathing medium leads to the development of a Cl- conductance in the basolateral membrane as long as some Na+ remains in the medium. However, cell swelling induced by mucosal dilution does not lead to the appearance of a Cl- conductance. Thus the activation of this conductance requires both swelling and membrane depolarization. These results show that 1) high mucosal K+ leads to cell swelling due to the entry of Cl- along with K+ and the Cl- can enter across either membrane, 2) the Cl- pathways require the presence of mucosal Na+, and 3) cell volume regulation is activated by an increase in volume per se, i.e., a hyposmotic exposure is not required for volume regulation to occur.

Animals↗
PubMed1989

Electrophysiological effects of mucosal Cl- removal in Necturus gallbladder epithelium.

The factors responsible for the cell membrane hyperpolarization elicited in Necturus gallbladder epithelium on Cl- removal from the mucosal bathing solution were evaluated with conventional and ion-sensitive microelectrode techniques. Cl- removal causes reversal of apical Cl- -HCO3- exchange, resulting in a fall in intracellular Cl- activity (aiCl) and an increase in intracellular pH (pHi). Concomitantly, the cell membranes hyperpolarize to values close to the K+ equilibrium potential (EK), aiNa falls, and aiK rises. The observed changes in membrane voltage are not attributable to a pHi-dependent increase in cell membrane K+ permeability (PK), because 1) the cell membrane resistances increased and 2) elevating solution partial pressure of CO2 (PCO2) to counterbalance the cellular alkalinization on mucosal Cl- removal caused a further hyperpolarization of the cell membranes to values greater than EK. This additional hyperpolarization was related to the activity of the Na+ pump, inasmuch as it was accompanied by an increase in aiNa and was ouabain sensitive. These results are consistent with, but do not prove, pump electrogenicity. During the period of Cl- removal from the mucosal bathing solution, the cell membrane depolarization caused by raising serosal K+ concentration was increased, whereas the depolarization caused by lowering serosal Cl- concentration was decreased, compared with substitutions under control conditions. These results indicate that mucosal Cl- removal causes a decrease in basolateral PCl, which we speculate could be due to a decrease in cell volume. We conclude that the hyperpolarization of the cell membranes on mucosal Cl- removal is primarily due to the combined effects of the fall in basolateral PCl and the increase in basolateral ECl.

Animals↗
PubMed1990

Mechanisms underlying volume regulatory decrease by Necturus gallbladder epithelium.

Volume regulatory decrease (VRD) by Necturus gallbladder epithelial cells in Cl Ringer was unaffected by the addition of 5 mM BaCl2 to apical perfusates but was inhibited by the addition of 5 mM BaCl2 and 50 or 3 microM phencyclidine (PCP) to serosal perfusates, suggesting that K channels in the basolateral membrane were activated during VRD. VRD was unaffected by replacement of Cl with NO3 or SCN, suggesting that Cl-dependent Na-K-Cl and K-Cl cotransport were not involved. In SCN Ringer, VRD was inhibited by the addition of 0.1 mM bumetanide to serosal perfusates, suggesting that bumetanide-sensitive anion channels in the basolateral membrane were also activated. A transient 10-mV hyperpolarization of the membrane potential was associated with VRD. The channel blockers that inhibited VRD had little or no effect on the hyperpolarization, suggesting that the changes in membrane potential were unrelated to the changes in cell volume. Perfusion of the apical surface of the epithelium with isotonic solutions containing 10 mM D-glucose resulted in a variable increase in cell volume followed by a variable shrinkage to normal, suggesting that VRD was also activated during organic solute absorption. The increase in cell volume was blocked by the addition of 0.01 or 1 mM phlorizin to mucosal perfusates. The reduction in cell volume was inhibited by the addition of 0.1 mM bumetanide, but not BaCl2 or PCP, to serosal perfusates, indicating the the shrinkage mechanism secondary to glucose addition differed from that seen after exposure to hypotonic perfusates.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1994

Regulation of NaCl entry into Necturus gallbladder epithelium by protein kinase C.

The role of protein kinase C in the regulation of the mode of NaCl entry into Necturus gallbladder epithelial cells was determined from the rate and magnitude of ouabain-induced cell swelling in the presence of inhibitors. Stimulation of protein kinase C by phorbol ester increased the rate of cell swelling from the control value of 2.9% to 4.7%/min and caused the predominant apical membrane transport mechanism for NaCl to switch from bumetanide-sensitive Na-Cl cotransport to amiloride-sensitive parallel exchange. Na-Cl cotransport could be restored as the predominant mode of NaCl entry by treatment of stimulated tissues with the kinase inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and calphostin C. Therefore the mechanism of NaCl transport across the apical membrane can be controlled by the activity of protein kinase C.

Animals↗
PubMed1995

Reconstitution of a KATP channel from basolateral membranes of Necturus enterocytes.

We have previously reported that basolateral membrane vesicles isolated from Necturus maculosa small intestinal epithelial cells and incorporated into planar phospholipid bilayers display a highly selective "maxi"-conductance K+ channel whose open-time probability is affected by voltage. We now report that this channel is inhibited by MgATP in the solution bathing the intracellular face of the channel but not by Mg2+ or the Na+ or K+ salts of ATP; the effects of MgATP can be prevented or reversed by MgADP. The channel is also inhibited by the nonhydrolyzable ATP analogue magnesium adenosine 5'-O-(3-thiotriphosphate) and the sulfonylurea derivatives tolbutamide and glibenclamide; all of these agents are effective in the intracellular compartment but not when added to the extracellular compartment alone. Channel activity is stimulated by the "K+ channel opener," diazoxide, which also reverses the effect of glibenclamide but not of MgATP. The possible role of this channel as a mediator of the parallelism between basolateral membrane Na(+)-K+ pump activity and the macroscopic K+ conductance of that barrier is discussed.

Adenosine Diphosphate↗
PubMed1998

Colocalization of glycolytic enzyme activity and KATP channels in basolateral membrane of Necturus enterocytes.

86Rb fluxes through ATP-regulated K+ (KATP) channels in membrane vesicles derived from basolateral membranes of Necturus small intestinal epithelial cells as well as the activity of single KATP channels reconstituted into planar phospholipid bilayers are inhibited by the presence of ADP plus phosphoenolpyruvate in the solution bathing the inner surface of these channels. This inhibition can be prevented by pretreatment of the membranes with 2, 3-butanedione, an irreversible inhibitor of pyruvate kinase (PK) and reversed by the addition of 2-deoxyglucose plus hexokinase. The results of additional studies indicate that PK activity appears to be tightly associated with this membrane fraction. These results, together with considerations of the possible ratio of Na+-K+ pumps to KATP channels in the basolateral membrane, raise the possibility that "cross talk" between those channels and pumps (i.e., the "pump-leak parallelism") may be mediated by local, functionally compartmentalized ATP-to-ADP ratios that differ from those in the bulk cytoplasm.

Adenosine Diphosphate↗
PubMed1999

Extracellular ATP stimulates volume decrease in Necturus red blood cells.

This study examined whether extracellular ATP stimulates regulatory volume decrease (RVD) in Necturus maculosus (mudpuppy) red blood cells (RBCs). The hemolytic index (a measure of osmotic fragility) decreased with extracellular ATP (50 microM). In contrast, the ATP scavenger hexokinase (2.5 U/ml, 1 mM glucose) increased osmotic fragility. In addition, the ATP-dependent K+ channel antagonist glibenclamide (100 microM) increased the hemolytic index, and this inhibition was reversed with ATP (50 microM). We also measured cell volume recovery in response to hypotonic shock electronically with a Coulter counter. Extracellular ATP (50 microM) enhanced cell volume decrease in a hypotonic (0.5x) Ringer solution. In contrast, hexokinase (2.5 U/ml) and apyrase (an ATP diphosphohydrolase, 2.5 U/ml) inhibited cell volume recovery. The inhibitory effect of hexokinase was reversed with the Ca2+ ionophore A-23187 (1 microM); it also was reversed with the cationophore gramicidin (5 microM in a choline-Ringer solution), indicating that ATP was linked to K+ efflux. In addition, glibenclamide (100 microM) and gadolinium (10 microM) inhibited cell volume decrease, and the effect of these agents was reversed with ATP (50 microM) and A-23187 (1 microM). Using the whole cell patch-clamp technique, we found that ATP (50 microM) stimulated a whole cell current under isosmotic conditions. In addition, apyrase (2.5 U/ml), glibenclamide (100 microM), and gadolinium (10 microM) inhibited whole cell currents that were activated during hypotonic swelling. The inhibitory effect of apyrase was reversed with the nonhydrolyzable analog adenosine 5'-O-(3-thiotriphosphate) (50 microM), and the effect of glibenclamide or gadolinium was reversed with ATP (50 microM). Finally, anionic whole cell currents were activated with hypotonic swelling when ATP was the only significant charge carrier, suggesting that increases in cell volume led to ATP efflux through a conductive pathway. Taken together, these results indicate that extracellular ATP stimulated cell volume decrease via a Ca2+-dependent step that led to K+ efflux.

Adenosine Triphosphate↗
PubMed2000

Effect of HCO(3)(-) on TPA- and IBMX-induced anion conductances in Necturus gallbladder epithelial cells.

Effects of HCO(3)(-) on protein kinase C (PKC)- and protein kinase A (PKA)-induced anion conductances were investigated in Necturus gallbladder epithelial cells. In HCO(3)(-)-free media, activation of PKC via 12-O-tetradecanoylphorbol 13-acetate (TPA) depolarized apical membrane potential (V(a)) and decreased fractional apical voltage ratio (F(R)). These effects were blocked by mucosal 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), a Cl(-) channel blocker. In HCO(3)(-) media, TPA induced significantly greater changes in V(a) and F(R). These effects were blocked only when NPPB was present in both mucosal and basolateral compartments. The data suggest that TPA activates NPPB-sensitive apical Cl(-) conductance (g(Cl)(a)) in the absence of HCO(3)(-); in its presence, TPA stimulated both NPPB-sensitive g(Cl)(a) and basolateral Cl(-) conductance (g(Cl)(b)). Activation of PKA via 3-isobutyl-1-methylxanthine (IBMX) also decreased V(a) and F(R); however, these changes were not affected by external HCO(3)(-). We conclude that HCO(3)(-) modulates the effects of PKC on g(Cl)(b). In HCO(3)(-) medium, TPA and IBMX also induced an initial transient hyperpolarization and increase in intracellular pH. Because these changes were independent of mucosal Na(+) and Cl(-), it is suggested that TPA and IBMX induce a transient increase in apical HCO(3)(-) conductance.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Microelectrode studies of Necturus antral mucosa: electrical potentials and resistances.

Intracellular microelectrode techniques were applied to Necturus antral mucosa. Stable intracellular impalements were obtained with 15-50 M omega microelectrodes filled with 3M KCl. It was possible to change rapidly the mucosal bathing solution while maintaining the microelectrode in the cell. With these techniques, we were able to measure the electrical potentials and resistances of the cell membranes and the shunt pathway. The transepithelial potential was -4.9 +/- 1.3 mV, serosal solution reference. Apical cell membrane potential was -43.9 +/- 0.6 mV, cell negative to the mucosal solution. Basolateral cell membrane potential was -48.8 +/- 1.3 mV, cell negative to serosal solution. Transepithelial resistance was 427 +/- 66 omega . cm2. The ratio of apical to basolateral membrane resistances was 3.4 +/- 0.3. The electrical resistances of the transcellular and paracellular pathway were determined by the measurement of the total transepithelial resistance and the ratio of apical to basolateral cell membrane resistances before and after blocking apical membrane sodium permeability with amiloride. The resistances of the apical cell membrane, basolateral cell membrane, and the shunt were 2,203 +/- 585, 1,296 +/- 384, and 604 +/- 81 omega . cm2, respectively (mean +/- SE). Calculations from these measurements indicate that the shunt contribution to transepithelial conductance was approximately 85%.

Amiloride↗
PubMed1985

Microelectrode studies of Necturus antral mucosa. II. Equivalent circuit analysis.

Intracellular microelectrode techniques were employed to determine the equivalent circuit parameters in Necturus antral mucosa. Stable intracellular impalements were obtained using 15- to 50-M omega microelectrodes. Measured transepithelial and cellular potentials and voltage deflections produced by transepithelial current pulses were used to calculate the electrical resistances of the cell membranes and the equivalent electromotive forces (EMF) at both cell borders. The measured potentials were -4.1 +/- 0.8 mV for the entire epithelia, -41.8 +/- 5.1 mV for the apical membrane, and -45.9 +/- 5.0 mV for the basolateral membrane. Values for the resistances were 7,300 +/- 1,900 omega X cm2 for the apical, 3,990 +/- 1,170 omega X cm2 for the basolateral, and 710 +/- 40 omega X cm2 for the shunt. Assuming that the shunt EMF is zero with control Ringer solution on both sides of the tissue, the effect of this relatively low-resistance shunt on electrical parameters can be determined. The cell membrane EMFs are both oriented with the interior negative and are -1.2 +/- 9.7 mV (apical) and -69.7 +/- 11.3 mV (basolateral). The difference between these values and the measured potentials is the result of a flow of current through the shunt from serosa to mucosa, hyperpolarizing the apical and depolarizing the basolateral membranes.

Amiloride↗
PubMed1987

Effects of luminal salt concentration on electrical pathways in Necturus antrum.

By use of microelectrode techniques the electrical resistances of the cell membranes and paracellular pathways of surface epithelium in Necturus antrum were determined under control conditions (Ringer solutions containing 106.6 mM Na+, 91.4 mM Cl-) and during exposure to mucosal solutions containing high Na+ and Cl- concentrations. Resistances were determined by briefly exposing tissues to mucosal solutions containing 10(-4) M amiloride, a reversible inhibitor of Na+ conductances. Under control conditions in eight tissues, measurements obtained by exposure to amiloride were not significantly different from those obtained by an independent method, intraepithelial cable analysis, thus indicating the validity of the measurements obtained by the amiloride method. In 10 tissues, high luminal NaCl concentrations (Ringer salts + 125 mM NaCl) increased the apical cell membrane resistance from 5,778 +/- 267 to 7,714 +/- 422 omega X cm2 (P less than 0.01) and the basolateral membrane resistance from 2,973 +/- 186 to 3,869 +/- 335 omega X cm2 (P less than 0.01). The resistance of the paracellular pathway decreased from 625 +/- 13 to 505 +/- 13 omega X cm2 (P less than 0.001). Similar alterations in these resistances were observed when Na+ or Cl- were increased individually, when added as salts of isethionate- and N-methyl-D-glucamine+, respectively. These effects were not attributable to increases in luminal osmolarity, since mucosal solutions made equally hyperosmotic with 250 mM sucrose elicited increases in paracellular pathway resistance and decreases in resistances of the cell membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1989

Effects of cations and pH on apical membrane potential of in vitro Necturus antrum.

The surface epithelial cells of the gastric mucosa transport Na+ from lumen to serosa. The first step in this process is the entry of Na+ through an amiloride-sensitive Na+ channel at the apical membrane. The exact function(s) of this Na+ transport are unknown, but it has been suggested that it might help the stomach to withstand an acid load. The present study was undertaken to examine the effects of low luminal pH and the alkali cations Li+, K+, Rb+, and Cs+ on the amiloride-sensitive Na+ permeability of the apical membrane of Necturus antral cells by measuring the changes in apical membrane voltage (Vmc) using conventional microelectrode techniques. Isosmolar replacement of luminal NaCl (pH 7.25) with LiCl caused a depolarization of the Vmc, a decrease in transepithelial resistance (Rt), and an increase in the transepithelial potential (Vmc), whereas replacement with KCl, RbCl, or CsCl caused a hyperpolarization of the Vmc, an increase in Rt, and a decrease in the Vmc. Luminal acidification from pH 7.25 to pH 3.00 caused very similar changes with all the cation solutions tested, hyperpolarizing the Vmc, increasing Rt, and reducing the Vmc to near 0 mV. Acidification of the luminal NaCl solution from pH 7.25 to pH 2.00 caused a progressive hyperpolarization of the Vmc similar to the effects seen with luminal amiloride (10(-4) M) in pH 7.25 NaCl solutions or luminal Na+-free (N-methyl-D-glucamine) Ringer at pH 7.25. These results demonstrate that 1) of the cations tested only Li+ can substitute for Na+ in maintaining the Vmc, and 2) external H ions (low luminal pH) block cation permeability of the apical membrane.

Amiloride↗
PubMed1990

Feeding induces lipid accumulation and increased Na+ transport in in vitro Necturus antrum.

We investigated the effects of feeding on lipid accumulation and transepithelial transport using in vitro Necturus gastric antral mucosae. Antra from fed Necturi were examined for lipid accumulation using light, fluorescence, histochemical, and electron microscopy. Ussing chambers were used for measurement of potential difference (PD), transepithelial resistance (Rt), short-circuit current (Isc), and unidirectional fluxes of 22Na+ and [3H]mannitol. Light microscopy of antra from 2-day postfed animals showed many intracellular lipid granules in surface mucous epithelial cells. These granules could be distinguished from other intracellular organelles by their high affinity for osmium and the lipid fluorescent probe Nile red. Glycoprotein cytochemical staining showed these granules to be distinct from the epithelial cell mucous granules. Electron microscopy showed the lipid granules to be part of a membranous reticular network. Two-day postfed animals also had a approximately 3.5-fold increase in amiloride-sensitive Isc and PD, a decrease in Rt, and an increased luminal-to-serosal Na+ fluxes. Transepithelial [3H]mannitol fluxes were low and remained unchanged in both fasted and 2-day postfed animals. After 2 days of feeding, the PD and Isc began to decrease followed by a secondary increase in Rt. Feeding Necturi a corn oil diet did not induce the appearance of either cellular lipid or alterations in Isc but produced a transient increase in Rt. Our data show that feeding (goldfish) to Necturi causes an increase in both lipid accumulation and amiloride-sensitive Na+ transport in gastric antral cells.

Amiloride↗
PubMed1994

Osmotic water flow pathways across Necturus gallbladder: role of the tight junction.

To explore the quantitative significance of passive water flow through tight junctions of leaky epithelia, transepithelial water flow rates were measured in Necturus gallbladder mounted in chambers. Osmotic flows generated by raffinose gradients were asymmetrical with the greater flow in the mucosal-to-serosal direction. In tissue fixed in situ, intercellular spaces were dilated during mucosal-to-serosal flow and closed during serosal-to-mucosal flow. Tight junctions were focally separated (blistered), which correlated with the magnitude of mucosal-to-serosal flow. Blisters were not observed during serosal-to-mucosal flow or in nontransporting gallbladders. In freeze-fracture replicas, blisters appeared as pockets between intramembranous strands. Protamine, which decreases electrical conductance and increases depth and complexity of the tight junction, reduced osmotic water flow by approximately 30% in the mucosal-to-serosal direction (100 mosmol/kg gradient) without altering serosal-to-mucosal flow. We suggest that in the steady state, at least 30% of osmotically driven water passes transjunctionally in the mucosal-to-serosal direction, but flow is transcellular in the serosal-to-mucosal direction. Directionally divergent pathways may account for flow asymmetry.

Animals↗
PubMed1996

Electrophysiological effects of cholinergic agonists in surface epithelium of Necturus gastric antrum.

Intracellular microelectrode techniques were used to characterize voltage and conductance properties of the basolateral membrane of surface epithelial cells in in vitro Necturus antral mucosa. Flux studies confirmed that this tissue secretes HCO3- under resting conditions and during response to cholinergic stimulation. In studies using intracellular microelectrodes, exposure to cholinergic agonists such as acetylcholine, bethanechol, or carbachol elicited an initial hyperpolarization followed by depolarization of the basolateral cell membranes associated with up to fourfold increases in basolateral membrane conductance. Effects of acetylcholine were dose dependent (10(-6) - 10(-4) M) and prevented by pretreatment of tissues with the nonselective muscarinic receptor blocker atropine. Some variation in this response to cholinergic stimulation was observed and appeared to be related to the season (fall/winter/early spring vs. late spring/summer). Despite such variability, circuit analysis and ion substitution studies indicated that the carbachol-induced increases in basolateral conductance were due to increases in conductance to K+ and Cl- . These increases in basolateral transport processes may serve to stabilize cell ion composition and membrane electrical properties during cholinergic stimulation of mucus and HCO3- secretions.

Acetylcholine↗