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PubMed1994

Role of Ca(+)-dependent K-channels in the membrane potential and contractility of aorta from spontaneously hypertensive rats.

1. Contractile responses to KCl and membrane potentials were determined in aortic rings from spontaneously hypertensive rats (SHR), normotensive Wistar rats (NWR) and Wistar Kyoto rats (WKY) both in the absence and in the presence of the Ca(2+)-dependent K-channel blockers, apamin and tetraethylammonium (TEA). 2. Compared to NWR, aortic rings from WKY and SHR were less reactive and their Ca2+ uptake after stimulation with K+ was decreased. 3. Smooth muscle cell membrane potentials were higher in aortae from SHR and WKY than in NWR aortae, whereas SHR had higher K+ and lower Na+ intracellular activities than WKY and NWR, suggesting overactivity of the Na+/K+ pump in the hypertensive animals. 4. Treatment with apamin caused depolarization of WKY and SHR aortae, and increased their contractile responses to the same level as those of the NWR. Treatment with TEA also caused depolarization of aortae from WKY and SHR, but in the SHR the depolarization induced by TEA was smaller than that produced by apamin and the contractile responses to KCl did not reach the level of those of aortae from NWR. 5. It is concluded that overactivity of Ca(2+)-dependent K-channels in aortae of WKY and SHR contributes to their higher membrane potentials and lower responsiveness to vasoconstrictor stimuli. In SHR, an overactive Na+/K+ pump is also present, and the contribution of apamin-sensitive Ca(2+)-dependent K-channels to the membrane potential and reactivity appears to be more relevant than that of TEA-sensitive channels.

Animals↗
PubMed1978

Effects of X-rays on cell membranes. I. Changes of membrane potential of L-cells.

Changes in the membrane potential of cultured L-929lcells were investigated after irradiation with doses ranging from 5-200 Gy. Immediately after irradiation a depolarisation is observed that is followed by a damped oscillation of the membrane potential and finally by a rapprochement to the control value. Whereas the magnitude of depolarisation does not show any dependence on irradiation dose, the time required to reach the control value again increases with increasing dose. Up to 10 Gy, the period of the first half-oscillation rises rapidly to about 12 min, at higher doses a slow linear increase follows reaching a value of 23 min after 200 Gy.

Cell Membrane↗
PubMed1975

The effects of cholecystokinin-pancreozymin, acetylcholine and secretin on the membrane potentials of mouse pancreatic cells in vitro.

Cell membrane potentials in an in vitro preparation of mouse pancreas have been measured and the effects of cholecystokinin-pancreozymin, acetylcholine and secretin studied. The membrane potential-frequency histogram has four distinct peaks and was split into the sum of four Gaussian distributions with means of minus 14, minus 23, minus 32 and minus 41mV. The minus 32 mV peak is attributed to acinar cells which respond to cholecystokinin-pancreozymin or acetylcholine by depolarising to minus 15 to minus 20 mV, the response lasting up to 10 min. The minus 23 and minus 41 mV peaks are due to duct cells. A duct cell has a resting membrane potential of minus 23 mV and hyperpolarises to minus 41 mV in response to secretin stimulation, the response lasting for longer than 15 min. Duct cells regardless of their position in the duct system function electrophysiologically in identical fashion. The secretory sites for enzyme and electrolyte are distinct, the duct cells secrete only electrolyte while the acinar cells secrete only enzymes.

Acetylcholine↗
PubMed1980

Carbon dioxide, membrane potential and intracellular potassium activity in frog skeletal muscle.

1. The membrane potential of isolated frog muscle fibres has been measured in absence and in presence of CO2, at constant external pH. 2. At a normal external Cl concentration, CO2 (PCO2 = 97 mmHg; pH = 7.0) applied for 10 min caused a highly variable depolarization, the average potential change being 8 mV after 5 min. The effect was reversible 3. In Cl-free solutions, CO2 (PCO2 = 97 mmHg; pH = 7.0) caused a biphasic depolarization of 20 mV after 5 min. The effect was fully reversible on CO2 removal. 4. The same effect appeared at a lower partial pressure (PCO2 = 38 mmHg; pH 7.3) in the presence of tetrodotoxin (10(-7) M). 5. In order to investigate the cause of the CO2-induced depolarization, membrane potential and intracellular K activity (ai/K,)( of surface muscle fibres were measured with voltage and ion-sensitive micro-electrodes. 6. At a normal external Cl concentration, CO2(PCO2 approximately equal to 97 mmHg; pH = 7.0) decreased ai/K by 5 mM after 5 min. 7. The same effect appeared at low external Cl concentration (11 mM). 8. At high partial pressure (PCO2 approximately equal to 588 mmHg; pH = 6.8), CO2 reduced ai/K by 19 mM in 10 min. 9. In long-term experiments performed over 4 h with a normal external Cl concentration, CO2 (PCO2 approximately equal to 97 mmHg; pH 5.8 or 7) changed practically neither membrane potential, nor ai/K. 10. It is concluded that increasing the PCO2 when keeping the external pH constant causes an early depolarization of muscle. This effect is particularly marked in the absence of chloride. It can be explained partly, in surface muscle fibres, by a decrease of the intracellular K activity.

Animals↗
PubMed1997

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II.

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

Angiotensin II↗
PubMed1984

Resolution of cellular compartments involved in membrane potential changes accompanying IgE-mediated degranulation of rat basophilic leukemia cells.

The overall membrane potential of rat basophilic leukemia cells (RBL-2H3) calculated from the transmembrane distribution of the lipophilic, tritium-labelled cation tetraphenyl-phosphonium [( 3H]TPP+) was resolved into its mitochondrial and plasma membrane potential components. Using the mitochondrial uncoupler carbonylcyanide-p-trifluormethoxyphenyl hydrazone (FCCP) which collapses the mitochondrial potential, it was shown that about one third of the overall potential resulted from the mitochondrial contribution. Degranulation of the RBL cells induced by two different IgE-cross-linking agents (specific antigen and anti-IgE antibodies), was accompanied by, and well correlated with, a decrease in the overall potential. However, evaluation of the source of these observed potential changes revealed that the FCCP-insensitive fraction of the overall potential, delta psi P, (representing the plasma membrane potential), was not affected. In contrast, the FCCP-sensitive component due to the mitochondrial potential decreased when receptor cross-linking increased. Thus, the observed decrease in the overall potential is most probably a secondary event in the sequence leading from stimulus to secretion. Indeed, exposure of the RBL cells either to a high external concentration of K+ ions or to a high amount of external TPP+, both causing depolarization, failed to trigger degranulation. It is suggested that the apparent decrease in the measured overall potential is a reflection of the mitochondrial membrane depolarization. The latter is most probably caused by mitochondrial Ca2+ uptake initiated by the increase in the intracellular concentration of Ca2+ which follows cells activation.

Animals↗
PubMed1980

Na+-Ca2+ exchange is affected by membrane potential in cardiac sarcolemmal vesicles.

The effect of membrane potential on the Na+-Ca2+ exchange activity of isolated sarcolemmal vesicles from dog ventricles is examined. Na+-Ca2+ exchange is monitored as Nai+-dependent Ca2+ uptake as described by Reeves and Sutko ((1979) Proc. Natl. Acad. Sci. U. S. A. 76,590-594). Membrane potential is controlled by varying internal and external K+ in the presence of valinomycin. Inside-positive potentials stimulate Nai+-dependent Ca2+ influx. This stimulation is independent of Ca2+ concentration. The results indicate that Na+-Ca2+ exchange by itself can generate a substantial potential (approximately -60mV) in the sarcolemmal vesicles. The data are consistent with an electrogenic Na+-Ca2+ exchange mechanism in which three or more Na+ are exchanged for one Ca2+. This electrogenic exchange may have important implications in the control of myocardial tension development.

Animals↗
PubMed1991

The high and low affinity transport systems for dipeptides in kidney brush border membrane respond differently to alterations in pH gradient and membrane potential.

The principal aim of the present study was to investigate the effects of variation in proton gradient and membrane potential on the transport of glycyl-L-glutamine (Gly-Gln) by renal brush border membrane vesicles. Under our conditions of transport assay, Gly-Gln was taken up by brush border membrane vesicles almost entirely as intact dipeptide. This uptake was mediated by two transporters shared by other dipeptides and characterized as the high affinity (Kt = 44.1 +/- 11.2 microM)/low capacity (Vmax = 0.41 +/- 0.03 nmol/mg protein/5 s) and low affinity (Kt = 2.62 +/- 0.50 mM)/high capacity (Vmax 4.04 +/- 0.80 nmol/mg protein/5 s) transporters. In the absence of a pH gradient, only the low affinity system was operational, but with a reduced transport capacity. Imposing a pH gradient of 1.6 pH units increased the Vmax of both transporters. Kinetic analysis of the rates of Gly-Gln uptake as a function of external pH revealed Hill coefficients of close or equal to 1, indicating that transporters contain only one binding site for the interaction with external H+. The effects of membrane potential on Gly-Gln uptake were investigated with valinomycin-induced K+ diffusion potentials. The velocity of the high affinity system but not of the low affinity system increased linearly with increasing inside-negative K+ diffusion potentials (p less than 0.01). The Kt of neither system was affected by alterations in either pH gradient or membrane potential. We conclude that (a) the high affinity transporter is far more sensitive to changes in proton gradient and membrane potential than the low affinity transporter and (b) in the presence of a pH gradient, transport of each dipeptide molecule requires cotransport of one hydrogen ion to serve as the driving force.

Animals↗
PubMed1987

Maxi K+ channels in leaky epithelia are regulated by intracellular Ca2+, pH and membrane potential.

We have studied a Ca2+-activated K+ channel in the ventricular membrane of the epithelium of choroid plexus by means of the patch-clamp technique, using excised inside-out patches. The channel was highly K+ selective. It had a conductance of approximately 200 pS with 112 mM KCl on both sides of the membrane. The probability for the channel being open increased with intracellular Ca2+, pH and with membrane potential. The channel shows two gating modes. The primary gating mode has open and closed times which depend strongly on membrane potential, intracellular Ca2+ and pH. It accounts for the variation of the channel open probability. Lowering intracellular pH from 7.4 to 6.4 reduced the channel open probability mainly by increasing the channel closed time. It appears, that H+ can compete with Ca2+ in binding to the same site, thereby preventing channel opening. A second gating mode consisted of short-lived closures, or flickers. The open and closed time for this process were largely independent of membrane potential, intracellular Ca2+ and pH. The channel density was approximately 0.4 micron-2 corresponding to a K+-permeability of 2.2 10(-5) cm s-1 if the channels were fully open. In cell-attached patches we measured the open probability of the channel in the intact cell membrane. The channel is almost totally closed under normal cellular conditions. This type of channel is therefore not the membrane component that forms the electrodiffusive pathway for K+-ions.

Animals↗
PubMed1999

An equation describing spread of membrane potential changes in a short segment of blood vessel.

The spread of membrane potential changes throughout certain cells and tissues plays an important role in their physiology. The attenuation of such changes in any tissue is usually characterized by the cable length constant lambda, which can be determined experimentally if the equations describing membrane potential spread in the tissue are known. Here we derive an equation describing spread of membrane potential changes in a short cable, which is an appropriate model for short segments of blood vessels. This equation is more general than those already published in that the positions of both the current source that gives rise to a potential change, and the point at which the change is measured, can be anywhere along the cable.

Animals↗
PubMed1989

Ultraviolet radiation induces a change in cell membrane potential in vitro: a possible signal for ultraviolet radiation induced alteration in cell activity.

The regulation of a transmembrane ionic gradient, reflected by the cellular membrane potential, has been shown in several cell systems to be involved in the regulation of cell function. This investigation presents evidence that biologically relevant doses of ultraviolet radiation (UVR) will alter the membrane potential of keratinocytes in vitro. Estimation of the relative change in the steady-state membrane potential of the murine keratinocyte cell line PAM 212, the murine myelomonocytic cell line P388D1, and normal human keratinocytes in culture, were made through the use of the lipophilic cationic membrane potential sensitive probe; triphenylmethylphosphonium. Our observations indicate that UVR composed primarily of UVB (280-320 nm) radiation at doses as low as 100 J/m2 can induce a depolarization in the murine cell lines and a hyperpolarization in human keratinocytes. Evidence suggests that this difference in the direction of the membrane potential response reflects a difference in Na+/K+ ATPase activity following UVR. These results suggest a possible mechanism for modulation of keratinocyte activity induced by UVR.

Cells, Cultured↗
PubMed1958

Effects of external ions on membrane potentials of a lobster giant axon.

The effects of varying external concentrations of normally occurring cations on membrane potentials in the lobster giant axon have been studied and compared with data presently available from the squid giant axon. A decrease in the external concentration of sodium ions causes a reversible reduction in the amplitude of the action potential and its rate of rise. No effect on the resting potential was detected. The changes are of the same order of magnitude, but greater than would be predicted for an ideal sodium electrode. Increase in external potassium causes a decrease in resting potential, and a decrease in potassium causes an increase in potential. The data so obtained are similar to those which have been reported for the squid giant axon, and cannot be exactly fitted to the Goldman constant field equation. Lowering external calcium below 25 mM causes a reduction in resting and action potentials, and the occasional occurrence of repetitive activity. The decrease in action potential is not solely attributable to a decrease in resting potential. Increase of external calcium from 25 to 50 mM causes no change in transmembrane potentials. Variations of external magnesium concentration between zero and 50 mM had no measurable effect on membrane potentials. These studies on membrane potentials do not indicate a clear choice between the use of sea water and Cole's perfusion solution as the better external medium for studies on lobster nerve.

Action Potentials↗
PubMed1984

Effect of aspirin on epithelial cell membrane potentials of gastric fundic mucosa.

The effects of aspirin on epithelial cell membrane potentials of Necturus fundic mucosa were examined by in vitro experiments according to intracellular microelectrode techniques. Stable intracellular impalements were obtained with 15 to 50 M-ohm microelectrodes filled with 3M KCl. In neutral mucosal solutions (pH 7.0) aspirin (5.0 mM) resulted in a significant increase in apical cell membrane potential (Vmc) from -36.7 +/- 1.5 mV to -43.3 +/- 2.3 mV (p less than 0.001) and basolateral cell membrane potential (Vcs) from -42.7 +/- 1.8 mV to -50.6 +/- 2.4 (p less than 0.001). This hyperpolarization of the cell was associated with an increase in transmucosal potential from -5.8 +/- 0.7 to -7.4 +/- 0.9 (p less than 0.05) and an increase in the ratio of apical to basolateral membrane resistances from 5.1 +/- 1.2 to 8.8 +/- 1.9 (p less than 0.05). These changes were consistent with an increase in potassium conductance induced by the salicylate anion. In acidic mucosal solutions (pH 4.5) aspirin caused a reduction in Vmc and Vcs. This hypopolarization of the cell membrane is consistent with acidification of the epithelial cells. These observations support the proposed mechanisms of aspirin injury: (1) back diffusion of H+ into the cells and (2) influx of the salicylate anions into the cells, which may interfere with intracellular metabolism.

Animals↗
PubMed1987

Ionic basis of membrane potential in developing ectoderm of the Xenopus blastula.

1. The membrane potential and permeabilities of blastomeres isolated from the ectoderm of stage 6-10 Xenopus blastulae have been investigated. The increase in membrane potential between stages 6 and 9, reported previously in intact embryos, is not clearly apparent in isolated cells. However, marked differences were observed between early and late stages. 2. The membrane specific resistance was high at all stages (100-300 k omega cm2) and increased from stage 6 to stage 9. This specific resistance is much higher than previous estimates of the permeability of newly formed membrane after fertilization and very different from values reported for differentiated cells. 3. The membrane Na-K pump activity has been measured at all stages by applying ouabain to the cells (10(-4) to 10(-3) M). The pump rate per unit surface area, calculated as the ratio of the ouabain-sensitive part of the resting potential to the specific resistance, decreased from stage 7 (about 0.19 microA/microF) to stage 9 (about 0.04 microA/microF). 4. The ouabain-insensitive part of the resting potential increased from stage 6 to 9. At all stages, the blastomeres were permeable primarily to K+; blastomeres at stage 9 were more sensitive to change of external K+ than at stage 7, suggesting an increase in K+ selectivity. 5. The membrane potential was very sensitive to external pH at all stages. External protons appeared to block the permeability to K+. At low pH, it was possible to demonstrate some permeability of early blastomeres to Na+. 6. At variable times after impalement, cells underwent an increase in K+ permeability of 5- to 10-fold. This seems to be due to ion leak from the intracellular electrode. 7. This dual membrane state was observed at all stages and it may explain some of the earlier reports of high K+ permeability.

Animals↗
PubMed1996

Effect of glutamate receptor ligands on mitochondrial membrane potential in rat dissociated cerebellar cells.

The effect of three different glutamate receptor ligands on mitochondrial membrane potential has been studied in rat pup dissociated cerebellar cells by measuring rhodamine 123 fluorescence. L-glutamate, NMDA (N-methyl-D-aspartate) and kainate (from 10(-8) to 10(-3) M) decreased in a concentration-dependent manner the mitochondrial membrane potential with EC50 values of 6.7 +/- 1.7, 3.8 +/- 0.5, and 37.4 +/- 14 microM, respectively. Dizocilpine ((+)MK 801) was able to inhibit the NMDA- and L-glutamate-induced decrease in rhodamine 123 fluorescence, while kainate-induced fluorescence-decreases were unaffected. However, 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX) totally prevented the effect of kainate on mitochondrial membrane potential, but failed to block the L-glutamate effect. It is concluded that, in our cell preparation, L-glutamate exerts its action mainly through NMDA-subtype receptors, and that Ca2+ and Na+ entry through ionotropic glutamate receptors could be responsible for an impairment of mitochondrial membrane potential.

Animals↗
PubMed1998

Effects of 8-bromo-cyclic GMP on membrane potential of single swine tracheal smooth muscle cells.

Cyclic GMP relaxes swine tracheal smooth muscle. Relaxation occurs because of decreases in intracellular calcium concentration ([Ca++]i) that are thought to occur through hyperpolarization which inhibits calcium influx. Activation of K+ channels has been suggested as the underlying mechanism for the hyperpolarization. In the present study, the effects of 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP, a membrane-permeable analog of cyclic GMP) on acetylcholine (ACh)-induced increases in [Ca++]i were examined by laser scanning confocal microscopy in fluo 3-loaded single cells. Membrane potential and currents were measured by the perforated-configuration of patch-clamp method, 8-Bromo-cGMP (1 microM-0.1 mM) inhibited 0.1 microM ACh-induced oscillations in [Ca++]i in a concentration-dependent manner. Spontaneous changes in membrane potential were observed by the patch-clamp method. Acetylcholine (0.03 microM) did not affect the time-averaged mean potential. The spontaneous changes in membrane potential were reduced and the cells were depolarized by 0.1 microM ACh and to a greater degree by 1 microM ACh. This result is consistent with previous observations of ACh-induced depolarization in intact tissue. The application of 0.1 mM 8-Br-cGMP had no significant effects on spontaneous changes in membrane potential and did not induce changes in membrane potential in cells treated with 0.1 microM ACh. In voltage-clamped cells, ACh (0.1 microM) induced oscillations in calcium-activated K+ currents. 8-Bromo-cGMP (0.1 mM) inhibited these ACh-induced oscillations in currents, but had no significant effects on spontaneous changes in membrane current in unstimulated cells. These data indicate that 8-Br-cGMP inhibits ACh-induced increases in [Ca++]i by mechanisms other than regulation of membrane potential.

Acetylcholine↗
PubMed2005

Ion channel regulation of the dynamical instability of the resting membrane potential in saccular hair cells of the green frog (Rana esculenta).

AIMS: We investigated the ion channel regulation of the resting membrane potential of hair cells with the aim to determine if the resting membrane potential is poised close to instability and thereby a potential cause of the spontaneous afferent spike activity. METHODS: The ionic mechanism and the dynamic properties of the resting membrane potential were examined with the whole-cell patch clamp technique in dissociated saccular hair cells and in a mathematical model including all identified ion channels. RESULTS: In hair cells showing I/V curves with a low membrane conductance flanked by large inward and outward rectifying potassium conductances, the inward rectifier (K(IR)), the delayed outward rectifier (K(V)) and the large conductance, calcium-sensitive, voltage-gated potassium channel (BK(Ca)) were all activated at rest. Under current clamp conditions, the outward current through these channels balanced the inward current through mechano-electrical transduction (MET) and Ca2+ channels. In 45% (22/49) of the cells, the membrane potential fluctuated spontaneously between two voltage levels determined by the voltage extent of the low membrane conductance range. These fluctuations were not influenced by blocking the MET channels but could be reversibly stopped by increasing [K+]o or by blocking of K(IR) channels. Blocking the BK(Ca) channels induced regular voltage oscillations. CONCLUSIONS: Two intrinsic dynamical instabilities of V(m) are present in hair cells. One of these is observed as spontaneous voltage fluctuations by currents through K(IR), K(V) and h-channels in combination with a steady current through MET channels. The other instability shows as regenerative voltage changes involving Ca2+ and K(V) channels. The BK(Ca) channels prevent the spontaneous voltage fluctuations from activating the regenerative system.

Animals↗
PubMed1979

Estimation of membrane potentials of individual lymphocytes by flow cytometry.

The membrane potentials of individual cells can be estimated by flow cytometric quantitation of the cells' uptake of the fluorescent lipophilic cationic dye 3,3'-dihexyloxacarbocyanine iodide. Human lymphocytes separated from peripheral blood on Hypaque-Ficoll gradients are uniformly depolarized by gramicidin and hyperpolarized by valinomycin. Concanavalin A and phytohemagglutinin depolarize only a fraction of the lymphocytes. The flow cytometric technique allows precise detection of heterogeneous membrane potential responses to stimuli such as lectins; it could also provide a basis for sorting cells that respond differently to a given stimulus.

Cations↗