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PubMed1981

Thyroid follicular cells: the resting membrane potential and the communication network.

Intracellular recordings of membrane potentials, input resistance and time constant have been made in vitro from the follicular cells of the rat, rabbit and guinea-pig thyroid glands using glass microelectrodes. The passive permeability properties of these cells have been investigated by altering the concentration of one or more ions in the superfusing fluid. Investigations into the intercellular coupling characteristics of the thyroid gland were made by inserting two microelectrodes into neighbouring communicating cells. The mean transmembrane potentials were between - 60 and - 70 mV in all three species studied. The magnitude of the membrane potential in the rat was found to be dependent mainly upon the gradient for potassium (K+) across the membrane. Current-voltage relationships were investigated in all three species by injecting rectangular de- or hyperpolarizing current pulses through the recording microelectrode. Within a relatively wide range (- 20 to - 80 mV), there was an approximately linear relationship between injected current and change in membrane potential. The input resistance was about 11 Momega in all three species, while the time constant (tau) varied from 5-35 ms. Readmitting K to K-deprived rat thyroids during intracellular microelectrode recording caused a transient hyperpolarization which was unaccompanied by any change in input resistance. The transient hyperpolarization was abolished by ouabain. Addition of 10(-3) M ouabain to the resting cell caused an immediate depolarization of approximately 2 mV. Electrical coupling between neighbouring cells could only be observed if the distance between the tips of the two exploring microelectrodes was less than 15 micrometer. The coupling coefficient (V2/V1) was close to 1. Assuming uniform current spread within one follicle and electrical isolation of individual follicles from each other the specific membrane resistance of the rat thyroid follicular cells was calculated to be 4.9 komegacm2.

Animals↗
PubMed1994

Functional and structural changes of isolated rat parietal cells during membrane potential modulation.

The present experiments were undertaken to extent our earlier observations (J Physiol Pharmacol 1991, 42, 367-79) relating membrane potential with membrane recycling of parietal cells. Studies were performed in vitro using gastric glands that were isolated through the use of rat stomachs transformed into "everted sacs" and filled with hyperosmolar NaCl-EDTA solution. Acid production was indirectly determined by accumulation of 14C-aminopyrine (AP) and its translocation by measurement of acridine orange fluorescence. H+/K(+)-ATPase activity was assayed by measurement of K(+)-stimulated p-nitrophenylphosphatase (pNPPase) of the proton pump. Morphologic state of parietal cells in relation to their functional activity was observed using electron microscopy. Changes in the membrane potential were obtained by the treatment of gastric glands with protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) in the incubation media of different pH. CCCP caused time-dependent decrease in AP accumulation by parietal cells from the medium of pH 6.6 but not that of pH 7.8. pNPPase activity increased in aplical and decreased in tubulovesical membrances prepared from CCCP treated glands which were incubated in the medium being more acidic than cell cytoplasm. Electron microscopic assessment showed morphological transformation of resting parietal cells treated with CCCP in pH 6.6 from nonsecreting to secreting state. CCCP acting in acidic incubation medium also caused the decrease in acridine orange fluorescence in the cytoplasm of parietal cells with some temporary increase of its fluorescence in the lumen o gastric glands. These findings support our hypothesis that changes in parietal cell membrane potential by protonophore CCCP may translocate HCl from tubulovesicles to secretory canaliculi. While the above explanation is suggestive, the exact mechanisms controlling a membrane recycling during the secretory response of parietal cells in vitro remain to be elucidated.

4-Nitrophenylphosphatase↗
PubMed1982

Fluorescence changes of rhodamine 6G associated with changes in membrane potential in synaptosomes.

The intensity of rhodamine 6G fluorescence was found to be a useful scale for measuring the membrane potential in synaptosomes. The fluorescence of rhodamine 6G in synaptosomal suspensions increases with depolarization in the synaptosomes induced by the replacement of cations in the medium or by the addition of agents known to depolarize the membrane potential. Considering the character of the dye, we have derived an equation which gives the relation between the fluorescence intensity of the dye and the membrane potential. The change in membrane potential (diffusion potential) of synaptosomes was calculated using the equation. The calculated membrane potential was proportional to the logarithm of the K+ concentration above 20 mM, and the slope of membrane potential against log [K+] was about 52 mV per decade of concentration. The permeability ratio (Px/Pk; the ratio of the permeability constants of a given cation, X+, and K+) was estimated from the calculated membrane potential.

Animals↗
PubMed1989

Kinetic model of the effects of electrogenic enzymes on the membrane potential.

Electrogenic enzymes contribute to the electrical field existing across biological membranes by using a source of free energy to generate an ionic current. The model introduced here permits one to evaluate this contribution. Since the model incorporates the electrogenic enzyme in the form of a sequential kinetic diagram, it permits one to study the kinetic effects of the concentration of the enzyme, the substrates and the different ligands on the membrane potential. Ionic electrodiffusion is expressed in terms of a chemical reaction; ionic permeabilities are thus treated as voltage-dependent rate constants. We use the condition of global electroneutrality to obtain an expression for the electrical potential difference across the membrane; such expression constitutes an extension of the Goldman-Hodgkin-Katz equation. The enzyme-related terms appear in the equation as functions of the rate constants and the diverse concentrations. The model is used to analyze the case of a cell membrane traversed by Na+ and K+ by simple diffusion, and by electrogenic transport mediated by a Na+-K+ ATPase. The enzyme reaction is represented by the six-step scheme proposed by Chapman et al. (1983, J. membr. Biol. 74, 139-153). The main results of the numerical calculations are that, within a certain interval, the membrane potential difference depends linearly on the enzyme density and hyperbolically on the ATP concentration. A similar behavior has been experimentally observed for the electrogenic proton pump of Neurospora crassa. Thus, the model here can be useful in the explanation and prediction of effects of electrogenic enzymes on the membrane potential.

Animals↗
PubMed1980

[Study of membrane potential of Bacillus subtilis and Escherichia coli cells by the penetration ions methods].

Using the penetrating ions of tetraphenylphosphonium (TPP+) and tetraphenylborone (TPB-), the membrane potential of the Bacillus subtilis and Escherichia coli cells was shown that the TPP+ absorption by the cells is an energy-coupled process. The TPB- anions are released from the cells after addition of an energy substrate. The value of the membrane potential calculated from the distribution pattern of the penetrating ions in the cells and the incubation medium lies within the interval of --100--150 mV (intracellular negative electric potential). The value of the membrane potential strongly depends on pH of the incubation medium; our attempts to measure the membrane potential in the E. coli cells at ph 6.0 were unsuccessful; however, at pH 8.5 it was found to be equal to --100 mV. Treatment of the cells with nigericin partially prevents the decrease of the membrane potential in an acidic medium and increases the potential in neutral and alkaline media. The formation of the membrane potential is suppressed by valinomycin and gramicidine, as well as by the oxidative phosphorylation uncouplers; the inhibiting effect of valinomycin requires the presence of K+ in the incubation medium. The membrane potential of the B. subtilis cells is insensitive to the effect of cyanide in the absence of arsenate. It is concluded that the membrane potential of B. subtilis and E. coli is formed both via respiration and by hydrolysis of intracellular ATP.

Bacillus subtilis↗
PubMed1984

A two sodium ion/D-glucose symport mechanism: membrane potential effects on phlorizin binding.

Apical membrane vesicles isolated from a continuous renal cell line, LLC-PK1, catalyze electrogenic Na+-stimulated hexose transport and Na+-dependent binding of 3H-labeled 1-[2-(beta-D-glucopyranosyloxy)-4, 6-dihydroxyphenyl]-3-(4-hydroxyphenyl)-1-propanone [( 3H]phlorizin), a competitive ligand of this transport system. Phlorizin was not itself transported across the membrane and thus can serve as a probe of the binding step. The stoichiometry of Na+-dependent phlorizin binding in vesicles was 1:1, whereas Na+/hexose cotransport in vesicles exhibited a 2:1 stoichiometry. Na+ increased the affinity of phlorizin binding without affecting the total number of binding sites. An increased number of Na+-dependent phlorizin binding sites was observed under conditions of interior-negative membrane potential. These results are consistent with a model of the Na+/glucose cotransport cycle in which the unloaded transporter is negatively charged and its orientation influenced by membrane potential. Glucose and one sodium ion interact with the transporter, resulting in an uncharged complex. Binding of a second sodium ion triggers translocation of glucose and both sodium ions via formation of a loaded carrier complex bearing a single positive charge.

Animals↗
PubMed1989

Membrane potential differences between adriamycin-sensitive and -resistant cells as measured by flow cytometry.

Using the fluorescent membrane potential probe, 3,3'-dihexyl-oxacarbocyanine (DiOC6(3], we found a 4-fold higher uptake in Adriamycin (ADM)-sensitive versus -resistant Friend leukemia cells (FLC). When sensitive cells were treated in the presence of high potassium (120 mM K+), there was a greater than 80% reduction of DiOC6(3) uptake. Using carbonylcyanide 4-trifluoromethoxy-phenylhydrazone (FCCP), a specific inhibitor of mitochondrial membrane potential, DiOC6(3) accumulation was reduced by less than 30% in these cells. Both results support the conclusion that a greater uptake of DiOC6(3) in ADM-sensitive than in -resistant cells indicates an increased plasma transmembrane potential. Since electronegative plasma membrane potentials are a driving force for the transport of lipophilic positively-charged compounds, differences in membrane potentials between sensitive and multiple drug resistant (MDR) tumor cells could have an important influence on drug accumulation and cytotoxicity. The drugs which our ADM-resistant FLC display multiple drug resistance to are positively charged. In MDR FLC, the calcium channel antagonist, verapamil, has been shown to block the efflux of Rhodamine 123 (Rho 123) and other positively-charged compounds. Since DiOC6(3) is also positively-charged, we used verapamil to investigate its effects on drug uptake. In MDR FLC, verapamil increased DiOC6(3) accumulation by 1.9-fold, whereas in sensitive cells it was increased 1.5-fold. In contrast, verapamil increased the levels of Rho 123 in resistant cells 7.8-fold but lowered them in sensitive cells 1.5-fold. The minimal loss of DiOC6(3) from both sensitive and MDR cells and the above results can best be interpreted as indicating that DiOC6(3) is not transported by the efflux "pump" system but that verapamil induces a plasma membrane potential increase in sensitive and resistant cells that DiOC6(3) is sensitive to. On the other hand, since Rho 123 did appear to be actively effluxed from these resistant cells, the enhancement of this compound by verapamil was more likely due to inhibition of the MDR "pump." How, or whether, plasma membrane potentials and the MDR efflux "pump" are related remains to be investigated. In the resistant cells, verapamil also induced an increase (13-fold) in the accumulation of the electrically neutral fluorescent probe for calcium, INDO-1/AM. However, verapamil had no effect on the efflux of this compound, which was equivalent in both resistant and sensitive cells. Thus, a new effect of verapamil on drug accumulation in MDR cells is identified here.

Animals↗
PubMed1973

Pancreatic acinar cells: ionic dependence of the membrane potential and acetycholine-induced depolarization.

1. Intracellular recordings of membrane potentials have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes.2. The mean membrane potential of the acinar cells during superfusion with Krebs-Henseleit solution was -39.2 mV. Increasing [K](o) tenfold decreased the membrane potential by 28 mV when [K](o) was above 10 mM. This depolarization was not affected by atropine (1.4 x 10(-6)M). Strophanthin-G (10(-3)M) slowly depolarized the cells at about 10 mV hr(-1).3. Brief exposure to acetylcholine (ACh), 5.5 x 10(-5)M, or pancreozymin resulted in a short lasting depolarization of the acinar cells. Atropine (1.4 x 10(-6)M) blocked the depolarizing action of ACh but not that of pancreozymin. Adrenaline (5.5 x 10(-5)M) or cyclic AMP (10(-3)-10(-4)M) did not influence the membrane potential.4. The amplitude of the ACh-induced depolarization was not dependent on the presence of CO(2)/HCO(3) in the bathing fluid, but it was closely dependent on the extracellular Na concentration. However, ACh was still able to evoke a small depolarization even after prolonged exposure of the tissue to a Na-free solution.5. During exposure of the tissue to a Ca-free solution the resting membrane potential was decreased and the ACh-induced depolarization was significantly reduced. Some substances which are known in other tissues to inhibit membrane Ca(2+) currents, i.e. La(3+), D-600 and tetracaine, were able to reduce, but never abolish, the ACh-induced depolarization.6. These results suggest that the effect of ACh on the pancreatic acinar cell is to increase the permeability of the membrane to commonly occurring ions with a consequent Na-influx and a small Ca-influx.

Acetylcholine↗
PubMed1984

Potassium distribution and membrane potential of sensory neurons in the leech nervous system.

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Effect of high pH on the plasma membrane potential and conductance in Elodea densa.

In leaves of Elodea densa the membrane potential measured in light equals the equilibrium potential of H+ on the morphological upper plasma membrane. The apoplastic pH on the upper side of the leaf is as high as 10.5-11.0, which indicates that alkaline pH induces an increased H+ permeability of the plasmalemma. To study this hypothesis in more detail we investigated the changes in membrane potential and conductance in response to alterations in the external pH from 7 (= control) to 9 or 11 under both light and dark conditions. Departing from the control pH 7 condition, in light and in dark the application of pH 9 resulted in a depolarization of the membrane potential to the Nernst potential of H+. In the light but not in the dark, this depolarization was followed by a repolarization to about -160 mV. The change to pH 9 induced, in light as well as in dark, an increase in membrane conductance. The application of pH 11, which caused a momentary hyper- or depolarization depending on the value at the time pH 11 was applied, brought the membrane potential to around -160 mV. The membrane conductance also increased, in comparison to its value at pH 7, as a result of the application of pH 11, irrespective of the light conditions.

Buffers↗
PubMed1982

Studies of the Ca2+ transport mechanism of human erythrocyte inside-out membrane vesicles. Evidence for the development of a positive interior membrane potential.

Previous observations on the effects of permeant anions on ATP-dependent calcium transport in inside-out vesicles prepared from human erythrocytes suggested that the calcium pump is electrogenic, generating a positive interior membrane potential. The present work demonstrates the development of a positive interior membrane potential across inside-out vesicle membranes during calcium transport in the absence of permeant anions. Several membrane potential probes, 1-anilino-8-naphthalenesulfonate, 3,3'-dipropylthiodicarbocyanine iodide, and an electron paramagnetic resonant triphenylphosphonium derivative, provide qualitative evidence for the development of a membrane potential. Moreover, a number of parallels are observed between the changes in the membrane potential measured by the probes and calcium transport. These include enhancement by calmodulin, time course of change, similar kinetic properties, and the requirement for intact vesicle membranes. Quantitative measurements of the membrane potential shows a positive interior membrane potential of 26-37 mV using radiolabeled permeant anion distribution and 38-57 mV using 3,3'-dipropylthiodicarbocyanine iodide fluorescence changes. These membrane potentials are of a similar magnitude to those reported for the sarcoplasmic reticulum calcium pump (Zimniak, P., and Racker, E. (1978). J. Biol. Chem. 253, 4631-4637).

Anilino Naphthalenesulfonates↗
PubMed2003

A state-dependent trigger for electrophysiological recording at predetermined membrane potentials.

This paper describes the circuitry and construction of a novel electronic threshold discriminator, and details its specific application to in vivo intracellular recording. The discriminator reliably triggers electrophysiological recording at pre-selectable membrane potentials in neuronal systems that exhibit membrane potential oscillations. It has been used successfully whilst recording from spiny projection neurons of the striatum to measure membrane properties and trigger electrical stimulation within either of two discrete membrane potential "states". The device works by comparing the analogue membrane potential waveform with a user-defined threshold membrane potential, and outputs a logic signal to flag the occurrence of a threshold-crossing event. This signal is used to trigger the commencement of episodic recording and the application of current injection or electrical stimulation at a consistent membrane potential. Thus, the discriminator acts as a functional clamp to isolate evoked responses from endogenous fluctuations in membrane potential. The unit uses cheap and easily available components and can be constructed with the minimum of electronics experience. It could be adapted to isolate discrete events within any oscillatory system.

Amplifiers, Electronic↗
PubMed1999

Endothelium-dependent blunted membrane potential responses to ATP-sensitive K+ channel modulators in aortae from rats with cirrhosis.

BACKGROUND/AIMS: In vivo studies have shown that arterial vasodilation induced by synthetic openers of ATP-sensitive K+ (K(ATP)) channels is decreased in rats with cirrhosis. Since vasodilation induced by these substances is mediated by membrane potential hyperpolarization in arterial smooth muscle cells, membrane potential hyperpolarization in response to K(ATP) channel openers may be altered in cirrhotic smooth muscle cells. The aim of the present study was to investigate the effects of K(ATP) channel modulators (i.e. openers and blockers of these channels) on the membrane potential in smooth muscle cells in isolated aortae from cirrhotic and normal rats. The influence of endothelin-1 production by endothelial cells on smooth muscle cells membrane potential responses to K(ATP) channel modulators was also studied. METHODS: Cells were impaled in situ (in intact and endothelium-denuded aortae) with a microelectrode that was used to measure membrane potentials. K(ATP) channel openers were diazoxide or cromakalim; blockers were glibenclamide or tolbutamide. Bosentan (a mixed endothelin receptor antagonist) and exogenous endothelin-1 were also used. Preproendothelin-1 mRNA was assayed in aortae by RNase protection assay. Aortic wall endothelin-1 concentration was measured by double antibody radioimmunoassay technique. RESULTS: As expected, in smooth muscle cells in intact normal aortae, K(ATP) channel openers induced membrane potential hyperpolarization and K(ATP) channel blockers membrane potential depolarization. In smooth muscle cells in intact cirrhotic aortae, K(ATP) channel openers and blockers did not significantly change the membrane potential. Endothelium removal or exposure of intact aortae to bosentan restored normal membrane potential responses to K(ATP) channel modulators in cirrhotic smooth muscle cells and did not alter the effects of these substances in normal smooth muscle cells. In endothelium-denuded aortae, exposure to exogenous endothelin-1 suppressed membrane potential responses to K(ATP) channel modulators. In intact aortae, the abundance of preproendothelin-1 mRNA and endothelin-1 did not significantly differ between normal and cirrhotic rats. CONCLUSIONS: K(ATP) channel opener-induced membrane hyperpolarization and K(ATP) channel blocker-elicited membrane depolarization are blunted in smooth muscle cells in intact cirrhotic aortae. This blunting is due to the activation of the endothelin-1 pathway in the aortic wall, downstream to the endothelial production of endothelin-1.

Adenosine Triphosphate↗
PubMed1976

Change in membrane potential during bacterial chemotaxis.

To find out if there are changes in membrane potential during bacterial chemotaxis, we measured the membrane potential of Escherichia coli indirectly by use of the permeating, lipid-soluble cation triphenylmethylphosphonium. Addition of attractants or repellents to the bacteria brought about a hyperpolarizing peak (as well as additional, later changes in membrane potential). This peak was shown to be a part of the chemotactic mechanism based on the following evidence: (i) All attractants and repellents tested gave this peak while chemotactically inert chemicals did not. (ii) Mutants lacking galactose taxis failed to give the peak with galactose but did with another attractant and with repellents. (iii) Methionine, required for chemotaxis, is also required for production of this peak. (iv) A mutant in a control gene )flaI), unable to synthesize flagella and cytoplasmic membrane proteins related to motility and chemotaxis, failed to give the peak. (v) Paralyzed (mot) mutants gave little or none of the peak. Generally nonchemotactic (che) mutants, on the other hand, did give this peak. Very likely there are ion fluxes that bring about this change in membrane potential. We discuss the possible role of the mot gene product as an ion gate controlled by a methylation-demethylation process in response to attractants and repellents acting through their chemoreceptors.

Chemotaxis↗
PubMed1989

[Effect of ethanol on synaptosomal membrane potential in the rat brain].

The membrane potential of rat brain synaptosomes was depolarized by ethanol at concentrations of over 0.8-1.6%. This ethanol-induced depolarization was augmented by 4-aminopyridine (4-AP) or the gluconate- -medium, but not affected by tetrodotoxin, choline-Cl, NH4Cl, picrotoxin, ethacrynic acid, furosemide or SCN- -medium. The ethanol-induced depolarization was augmented by 4-AP in Cl- - or gluconate- -medium, but not in SCN- -medium. These findings suggest that ethanol depolarizes the synaptosomal membrane potential through potassium and anion-related mechanisms, probably through potassium channels.

4-Aminopyridine↗
PubMed1983

The control of tonic tension by membrane potential and intracellular sodium activity in the sheep cardiac Purkinje fibre.

Intracellular Na activity (aiNa) was measured with recessed-tip, Na-selective micro-electrodes in voltage-clamped sheep cardiac Purkinje fibres. Tension was measured simultaneously. aiNa was increased reversibly either by exposing the preparation to K-free, Rb-free solution of by adding the cardioactive steroid strophanthidin. An increase of aiNa produced an increase of tonic tension which was larger at depolarized membrane potentials. At sufficiently negative membrane potentials, changes of aiNa (over the range 6-30 mM) had no effect on tonic tension. Therefore, both an increase of aiNa and a depolarization are required to increase tonic tension. It is concluded that either a low level of aiNa or a large negative membrane potential is sufficient to maintain a low intracellular Ca concentration. Tonic tension was measured as a function of aiNa. At a given membrane potential the relationship can be described empirically by an equation of the form: tonic tension = b(aiNa)y, where y is a constant and b depends on membrane potential. In five experiments y was found to be 3.7 +/- 0.7 (mean +/- S.E.M.) over a range of potentials from -60 to -10 mV. Tonic tension was measured as a function of membrane potential. At a given aiNa the relationship can be described approximately as: tonic tension = k exp (aV), where a is a constant and k depends on aiNa. In five experiments a was found to be 0.06 +/- 0.01 mV-1 (mean +/- S.E.M.). A depolarization of 10 mV increases tonic tension by the same amount as does an increase of aiNa that is equivalent to a 3.7 mV change of the Na equilibrium potential, ENa. Hence ENa is nearly 3 times more effective than membrane potential in controlling tonic tension. During a prolonged depolarization (several minutes) the initial increase of tonic tension decays gradually. This is associated with a fall of aiNa. The relationship between tonic tension and aiNa is similar to that seen when aiNa is increased by inhibiting the Na pump. It is concluded that the fall of aiNa is responsible for the decay of tonic tension. The changes of tonic tension reported in this paper are consistent with the effects of aiNa and membrane potential on a voltage-dependent Na-Ca exchange. The possibility that a voltage-dependent Ca channel contributes to tonic tension is also discussed.

Animals↗
PubMed1975

Pancreatic acinar cells: effect of acetylcholine, pancreozymin, gastrin and secretin on membrane potential and resistance in vivo and in vitro.

1. Intracellular recordings of membrane potential and input resistance have been made in vivo and in vitro from the exocrine acinar cells of rat pancreas using indwelling glass micro-electrodes. 2. The resting cell membrane potential and input resistance in the in vivo experiments were not markedly different from the values obtained in the in vitro experiments. The effect of both acetylcholine (ACh) and pancreozymin (CCK-Pz) on the pancreas in vivo as well as in vitro was to reduce both the acinar cell membrane potential and the input resistance narkedly. The amplitude of the evoked depolarization and the change in input resistance evoked by supramaximal stimuli were of the same magnitude in both types of preparations. 3. Gastrin had an effect on the acinar cell potential and resistance which was indistinguishable from that of CCK-Pz or ACh. The effect of gastrin or CCK-Pz was, in contrast to that of ACh, not influenced by the presence of atropine. The reversal potential for the gastrin evoked potential change was about -20 mV. 4. Secretin in doses producing maximal volume secretion in vivo had no effect on acinar cell membrane potential and input resistance. 5. Dibutyryl cyclic AMP (5mM) and cyclic GMP (1mM) had no effect on cell membrane potential or resistance. 6. It is concluded that the in vitro superfused pancreas segment preparation is a useful model system in electrophysiological studies since it functions essentially as the in vivo preparation. In contrast to both gastrin and CCK-Pz, secretin has no effect on the bioelectrical properties of the acinar cells, indicating that there are no physiologically important secretin receptors in rat acinar cells.

Acetylcholine↗
PubMed1973

Effects of electrogenic sodium pumping on the membrane potential of longitudinal smooth muscle from terminal ileum of guinea-pig.

1. The membrane potential of the separated longitudinal muscle of the guinea-pig terminal ileum was recorded intracellularly with glass micro-electrodes.2. In tissues kept at room temperature and then brought to 35 degrees C for 15-30 min or about 1 hr, the fall in membrane potential upon changing to potassium-free solution was 21.4 +/- 3.5 mV and 13.4 +/- 1.8 mV respectively. Ouabain (1.7 x 10(-6)M) produced a fall in membrane potential of 8.1 +/- 1.1 mV. Returning potassium to potassium-free solution, or changing from ouabain-containing to ouabain-free solution, resulted in an increase in membrane potential which was greater than the initial fall.3. Readmitting potassium to potassium-free solution produced an increase in membrane potential which began within 10 sec and reached a maximum within 15-30 sec. This response was reduced, abolished, or converted to a depolarization by ouabain. In chloride-deficient (13 mM) solution in which membrane resistance was increased, the response to readmitting potassium was increased 2(1/2)-fold so that the membrane potential sometimes exceeded -100 mV, which was probably more negative than E(K). On the basis of these results it was assumed that the response to readmitting potassium was due to the electrogenic activity of the sodium pump.4. The response to briefly readmitting a fixed concentration of potassium increased during the first 30 min in potassium-free solution. This increase was not due to an increase in membrane resistance as this fell with time in potassium-free solution. It was suggested that the increase in the response resulted from the progressive rise in internal sodium concentration which is known to occur in smooth muscle in potassium-free solution.5. Increasing the concentration of potassium over the range approximately 0.1-20 mM, increased the size of the electrogenic potential observed upon readmitting potassium to potassium-free solution. There was a fall in membrane resistance upon readmitting potassium (0.6, 5.9, or 20 mM) which was greater the larger the concentration of potassium. When allowance was made for the fall in membrane resistance, the dependency of the electrogenic response upon the concentration of potassium over the range 0.6-20 mM was much increased.6. The results indicate that the rate of electrogenic sodium pumping in this tissue is increased by increasing the external potassium concentration, and probably by increasing the internal sodium concentration. It was suggested that a rise in the latter could sensitize the pump to an increase in the former.

Animals↗