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At least 721 records · Page 40Linked to original sources
PubMed1987

Internal anion binding site and membrane potential dominate the regulation of proton pumping by the chromaffin granule ATPase.

Effects of anions and membrane potential on the reconstituted proton pump from chromaffin granules were investigated. When acetate was present inside of the vesicles, ATP-dependent proton uptake was absolutely dependent on external chloride. Without external chloride, however, substantial proton uptake was observed when chloride or sulfate was present inside of the vesicles. Inside negative membrane potential drove ATP-dependent proton uptake regardless of the anion species present inside or outside of the vesicles. It is concluded that the internal anion binding site and membrane potential regulate the proton pumping activity of the ATPase.

Acetates↗
PubMed1997

Characterization of delayed rectifier K+ currents in rabbit coronary artery cells near resting membrane potential.

Previous studies have suggested that delayed rectifier K+ (Kdr) channels contribute to the control of membrane potential in vascular smooth muscle. To explore this hypothesis further, we investigated the characteristics of Kdr channels in the negative voltage range in the rabbit coronary artery. The Kdr channel blocker 4-aminopyridine (1 mM) contracted intact vessels and depolarized them from -52 to -37 mV, suggesting that these channels significantly contribute to the maintenance of resting membrane potential. In contrast, the ATP-sensitive K+ channel blocker glybenclamide (3 microM) had little effect on resting tone and did not alter the contraction elicited with 4-aminopyridine. K+ currents in isolated cells were then investigated by using whole-cell patch-clamp techniques. Increasing extracellular K+ concentration ([K+]o) from 5 to 135 mM resulted in the appearance of large inward currents at potentials between -60 and 0 mV. The voltage dependence of conductance for inward K+ currents was steeper and shifted toward more negative potentials when compared with outward K+ currents in 5 mM [K+]o solution. Various blockers of Kdr channels, i.e., 4-aminopyridine (3 mM), phencyclidine (0.1 mM), and intracellular tetraethylammonium (10 mM), nearly abolished currents in high [K+]o solution. In contrast, Ba2+ (0.1 mM) was without effect. These results suggest that the inward currents detected at potentials between -60 and 0 mV in high [K+]o solution are Kdr currents. Our results suggest that Kdr channels physiologically contribute to the control of membrane potential in the rabbit coronary artery.

4-Aminopyridine↗
PubMed1983

Electron flow to dimethylsulphoxide or trimethylamine-N-oxide generates a membrane potential in Rhodopseudomonas capsulata.

Under dark and essentially anaerobic conditions electron flow to either dimethylsulphoxide or trimethylamine-N-oxide in cells of Rhodopseudomonas capsulata has been shown to generate a membrane potential. This conclusion is based on the observation of a red shift in the carotenoid absorption band which is a well characterised indicator of membrane potential in this bacterium. The magnitude of the dimethylsulphoxide- or trimethylamine-N-oxide-dependent membrane potential was reduced either by a protonophore uncoupler of oxidative phosphorylation or synergistically by a combination of a protonophore plus rotenone, an inhibitor of electron flow from NADH dehydrogenase. These findings, together with the observation that venturicidin, an inhibitor of the proton translocating ATPase, did not reduce the membrane potential, show that electron flow to dimethylsulphoxide or trimethylamine-N-oxide is coupled to proton translocation. Thus contrary to some previous proposals dark and anaerobic growth of Rps. capsulata in the presence of dimethylsulphoxide or trimethylamine-N-oxide cannot be regarded as purely fermentative.

Anaerobiosis↗
PubMed2000

[Membrane potential depolarization in the porcine ciliary epithelium evoked by nitric oxide].

BACKGROUND: The present work studies if in porcine ciliary body epithelium the intracellular signal transduction pathway nitric oxide (NO)--guanylate cyclase (GC)--3',5'-cyclic guanosinemonophosphate (cGMP) can change the membrane potential of the epithelium of the ciliary body. MATERIAL AND METHODS: Recordings of membrane potentials were done by means of intracellular microelectrodes in the presence of the NO donor Sodium Nitroprusside (SNP; 100 microM; n = 5) or the membrane permeable cGMP analogue 8-parachlorophenyl-thioguanosine-3',5' cyclic monophosphate (8-pCPT-cGMP; 100 microM; n = 5). To test whether the GC is involved in this process, recordings were repeated in both groups in presence or in absence of the GC inhibitor 1-H-(1,2,4)oxadiazole-(4,3-a)quinoxalin-1-one (ODQ; 10 microM; n = 4). RESULTS: SNP and 8-pCPT-cGMP both induced significant membrane potential depolarizations (7.7 +/- 1.8 mV and 13.1 +/- 1.3 mV, mean +/- SEM). Membrane depolarizations induced by SNP were significantly inhibited by ODQ (p < 0.01), whereas depolarizations induced by 8-pCPT-cGMP were not altered by the presence of ODQ (p > 0.2). CONCLUSIONS: Nitric oxide induces depolarizations of the membrane potential in the isolated porcine ciliary body. This process is transduced by activation of the GC. We conclude that nitric oxide might be involved in the regulation of permeability of the cellular membrane for ions in the ciliary body.

Animals↗
PubMed1993

Membrane potential determination in large unilamellar vesicles with hexakis(2-methoxyisobutylisonitrile)technetium(I).

The accumulation of the lipophilic cation hexakis (2-methoxyisobutylisonitrile)technetium (99mTc-MIBI) within large unilamellar vesicles made from egg phosphatidylcholine was examined as a function of time and membrane potential (Em). Equilibrium distribution occurred within minutes at 30 degrees C. The transmembrane distribution of Tc-MIBI was measured at Em = 0 mV and at a series of negative membrane potentials. The distribution of Tc-MIBI was in close agreement with the Nernst equation for passive distribution of a permeant ion across a bilayer, permitting the membrane potential to be predicted from Tc-MIBI distribution. In this respect, Tc-MIBI behaves similarly to other radioprobes of membrane potential, but with unique properties including high specific activity (10(9) Ci/mol), rapid kinetics of distribution, low potential-independent binding, and short half-life (6.02 h). The results indicate a mechanism for tissue accumulation of Tc-MIBI in vivo that may in part account for its utility in clinical imaging of ischemic myocardium.

Membrane Potentials↗
PubMed1998

Different effect of oxytocin on membrane potential of supraoptic oxytocin neurons in virgin female and male rats in vitro.

The effects of oxytocin on membrane potential were investigated in the supraoptic nucleus (SON) neurons of rats using whole-cell patch-clamp technique. SON neurons were electrophysiologically identified as oxytocin (OT) or vasopressin (VP) neurons. Application of OT (1 x 10[-7] M) hyperpolarized membrane potentials of OT neurons in virgin female rats but depolarized membrane potentials of putative OT neurons in male rats. The membrane conductance of SON neurons were increased by treatment of OT in both sexes, suggesting that OT increased the opening of channels on SON neurons. The reversal potential of OT neurons in virgin female rats and putative OT neurons in male rats under OT effective conditions were -66 +/- 1 mV (n = 4) and -46 +/- 2 mV (n = 5), respectively. These data suggest that OT released within the SON suppresses the activity of OT neurons in virgin female rats while it excites putative OT neurons in male rats.

Animals↗
PubMed1990

Membrane potential of rat calvaria bone cells: dependence on temperature.

The membrane potentials of bone cells derived from calvaria of new born rats was shown to be strongly dependent on temperature. When we lowered the temperature from 36 degrees C to 26 degrees C, cells with spontaneous resting membrane potentials (MP) of -80 to -50 mV depolarized (mean amplitude 8 mV; n = 33), and the membrane resistance increased by approximately 80% (n = 20). The temperature response depended on the actual MP, the reversal potential being in the range of -80 to -90 mV. With the application of ouabain (0.1-1 mmol/liter; n = 12), cells depolarized. Simultaneously, the reversal potential of the temperature response was shifted towards more positive values and approached the actual MP level of the cells. Consequently, the depolarization amplitudes induced by lowering temperature were reduced at spontaneous MP levels. The rise of the membrane resistance during cooling was unaffected. When the extracellular chloride concentration was reduced from 133 to 9 mmol/liter, temperature-dependent depolarizations persisted at spontaneous MP values (n = 5). The findings indicate that the marked effects of temperature changes on the MP of bone-derived cells are mainly determined by changes of the potassium conductance.

Alkaline Phosphatase↗
PubMed1979

Effect of membrane potential and internal pH on active sodium-potassium transport and on ATP content in high-potassium sheep erythrocytes.

Ouabain-sensitive Na+ and K+ fluxes and ATP content were determined in high potassium sheep erythrocytes at different values of membrane potential and internal pH. Membrane potential was adjusted by suspending erythrocytes in media containing different concentrations of MgCl2 and sucrose. Concomitantly either the external pH was changed sufficiently to maintain a constant internal pH or the external pH was kept constant with a resultant change of internal pH. The erythrocytes were preincubated before the flux experiment started in a medium which produced increased ATP content in order to avoid substrate limitation of the pump. It was found that an increased cellular pH reduced the rates of active transport of Na+ and K+ without significantly altering the ratio of pumped Na+/K+. This reduction was not due to limitation in the supply of ATP although ATP content decreased when internal pH increased. Changes of membrane potential in the range between -10 and +60 mV at constant internal pH did not affect the rates of active transport of Na+ or K+.

Adenosine Triphosphate↗
PubMed1993

Force, membrane potential, and [Ca2+]i during activation of rat mesenteric small arteries with norepinephrine, potassium, aluminum fluoride, and phorbol ester. Effects of changes in pHi.

In activated rat mesenteric small arteries, the effect of pHi on force, membrane potential, and free cytosolic calcium ([Ca2+]i) was assessed. Arteries were mounted in a myograph for isometric force development, and [Ca2+]i, pHi, or membrane potential was measured simultaneously with force. During activation with norepinephrine, potassium, aluminum fluoride (AlF-4), and phorbol 12-myristate 13-acetate (PMA, a phorbol ester), the vessels depolarized and [Ca2+]i increased, although the ratio of force to [Ca2+]i was less during potassium activation than with the other types of activation. Changes in pHi, with a constant pHo, were induced with NH4Cl or by changing PCO2. In resting vessels, the effects of the changes in pHi on tension, membrane potential, and [Ca2+]i were negligible. In vessels activated with norepinephrine or AlF-4, alkalinization caused an acute decrease of tone, which could be explained by a decrease in [Ca2+]i consequent to repolarization of the membrane. In vessels activated with potassium or PMA, the effects of alkalinization were smaller. This is consistent with acute alkalinization, affecting steps proximal in the excitation-contraction coupling distal to activation of G proteins. Acidification caused a transient increase in tone and [Ca2+]i, irrespective of the mode of stimulation, without affecting the membrane potential. Ryanodine did not abolish the transient increase in tone and [Ca2+]i. Thus, acute intracellular acidification may induce tone by release of an intracellular ryanodine-insensitive calcium pool or by affecting transmembranal calcium flux although in a membrane potential-independent way.

Aluminum↗
PubMed1975

Effects of potassium ions and sodium ions on membrane potential of epithelial cells in rat duodenum.

1. Mucosal and serosal membrane potentials (Vm and Vs) of epithelial cells in rat duodenum were recorded together with the transmural potential differences (PDt). 2. The value of Vm in rat duodenum at 37 degrees C was about -53mV, being considerably greater than the values reported hitherto for the small intestine of various species. 3. When Cl- in the mucosal medium was partially replaced with SO42- at fixed mucosal Na+ and K+ concentrations ([Na+]m and [K+]m), the membrane potential was scarcely affected in the steady state several minutes after replacement, whereas marked changes in the potential were observed with varying [K+]m or [Na+]m. 4. As the mucosal K+ concentration increased at constant [Na+]m, Vm was gradually decreased (depolarization), together with the increase in PDt. Such a change in Vm caused by varying [K+]m obeys Nernst's equation in the range of [K+]m higher than about 60 mM. 5. At constant [K+]m, an increase in [Na+]m also caused the decrease of Vm for the lower [K+]m region, whereas Vm was not affected by such changes in [Na+]m in the range of [K+]m higher than approx. 60 mM. 6. The values of PNa/PK were obtained from the modified Goldman equation under an appropriate assumption. The ratio of the permeability coefficients markedly increases from zero to approx. 0.07 with a decrease in [K+]m.

Animals↗
PubMed1987

The Bulla ocular circadian pacemaker. II. Chronic changes in membrane potential lengthen free running period.

We have used intracellular recording to directly measure the effects of three experimental agents, light, elevated potassium seawater, and lowered sodium seawater on the membrane potential of the putative circadian pacemaker neurons of the Bulla eye. These agents were subsequently tested for effects on the free running period of the circadian pacemaker. We report that: 1. When applied to the eye, light and elevated potassium seawater depolarized the putative pacemaker neurons, while lowered sodium seawater hyperpolarized them. The membrane potential changes induced by these agents are sustained for at least one hour, suggesting that they produce persistent changes in the average membrane potential of the putative pacemaker neurons. 2. The amplitude of the membrane potential response to the depolarizing agents varies with the phase of the circadian cycle. Depolarizations induced by light and elevated potassium seawater are twice as large during the subjective night than they are during the subjective day. No significant difference was found in the response to lowered sodium seawater at different phases. 3. Continuous application of each of these agents caused a lengthening of the free running period of the Bulla eye. Constant light increased the period by 0.9 h, while the other depolarizing treatment (elevated potassium seawater) increased the free running period by 0.6 h. Both treatments increased the mean peak impulse frequency of treated eyes. The hyperpolarizing treatment also increased the period of the ocular pacemaker (+0.8 h), but had little effect on peak impulse frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

A noninvasive fluorimetric procedure for measurement of membrane potential. Quantification of the NADPH oxidase-induced depolarization in activated neutrophils.

The electrogenic activity of the NADPH oxidase is associated with depolarization of the plasma membrane in activated neutrophils. The magnitude and consequences of this depolarization, however, remain unknown. Neutrophils are not amenable to electrophysiological determinations of membrane potential by current clamp. Instead, the occurrence of depolarization has been inferred from the use of potential-sensitive fluorescent dyes. However, such dyes partition into intracellular organelles and may yield erroneous results, particularly because the NADPH oxidase resides largely in secretory granules, where it has been claimed to become activated. We confirmed the intracellular generation of oxidase products using dihydrorhodamine, which is converted to the fluorescent rhodamine 123 when oxidized. Rhodamine 123 accumulated inside endomembrane organelles in both neutrophils and in differentiated HL60 cells, where it co-localized with the primary granule marker CD63. To estimate the surface membrane potential without interference from organelles, we devised a method based on the voltage-driven uptake of Mn(2+) across the plasmalemma. The uptake of Mn(2+) through calcium release-activated channels was measured as the rate of Indo-1 fluorescence quenching in thapsigargin-treated cells. The rate of Mn(2+) influx was found to vary when the membrane potential was manipulated using conductive ionophores and also when the NADPH oxidase was activated. A calibration curve in the positive potential range was constructed using the Na(+) ionophore SQI-Pr. Using this calibration, the membrane potential of phorbol ester-activated neutrophils was found to reach +58 +/- 6 mV, a sustained depolarization of over 100 mV compared with the resting potential. The depolarization was greatly diminished when the NADPH oxidase was inhibited with diphenylene iodonium. Together, these results indicate that the NADPH oxidase can generate a large depolarization of the plasmalemma, which should suffice to activate a variety of voltage-gated channels, including the outwardly rectifying H(+) conductance.

Membrane Potentials↗
PubMed2004

The effects of K+ channels modulators terikalant and glibenclamide on membrane potential changes induced by hypotonic challenge of guinea pig ventricular myocytes.

Contribution of inward rectifier K(+) currents (I(K1)) and ATP-sensitive K(+) currents (I(KATP)) to membrane potential changes of ventricular myocytes appearing during hypotonic challenge is unclear. We used here the whole cell patch clamp technique, voltage and current clamp modes, to record membrane potentials and ionic currents in isolated guinea pig ventricular myocytes under isotonic or hypotonic perfusion. The difference in osmolarity between iso- and hypotonic solutions was about 100 mOsm. Exposure to hypotonic solution for 60 s induced initial prolongation of action potential duration at 90% of repolarization (APD(90)) (from 176 +/- 10 to 189 +/- 11 ms, P<0.05, n = 13). Further perfusion for the next 300 s shorthened APD(90) to 135 +/- 9 ms (P<0.01, in comparison with control values, n = 13) and depolarized resting potential from -79.2 +/- 1.5 to -75.0 +/- 0.9 mV, (P<0.05, n = 13). Neither pretreatment with a blocker of I(K1) channels, terikalant at 10 microM, nor with a blocker of I(KATP) channels, glibenclamide at 1 microM, prevented the above-mentioned changes in membrane potential induced by hypotonic challenge when a pipette solution containing 5 mM ATP was used. Also, glibenclamide and terikalant did not affect the hypotonic-sensitive current, obtained by ramp or voltage-step protocols, respectively. Additionally, the current-voltage relationship (I-V curve) of the whole cell hypotonic-sensitive current shifted from an isotonic I-V curve in a parallel way. Our results indicate that I(K1) and I(KATP) do not participate in membrane potential changes induced by hypotonic solution at least in the guinea pig ventricular myocytes with sufficient intracellular ATP.

Animals↗
PubMed1987

Effect of membrane potential changes on the calcium transient in single rat cardiac muscle cells.

The mechanism that links membrane potential changes to the release of calcium from internal stores to cause contraction of cardiac cells is unclear. By using the calcium indicator fura-2 under voltage-clamp conditions, changes in intracellular calcium could be monitored in single rat ventricular cells while controlling membrane potential. The voltage dependence of the depolarization-induced increase in intracellular calcium was not the same as that of the calcium current (Isi), which suggests that only a small fraction of Isi is required to trigger calcium release from the sarcoplasmic reticulum. In addition, sarcoplasmic reticulum calcium release may be partly regulated by membrane potential, since repolarization could terminate the rise in intracellular calcium. Thus, changes in the action potential will have immediate effects on the time course of the calcium transient beyond those associated with its effects on Isi.

Animals↗
PubMed1985

Plasma membrane potential of neutrophils generated by the Na+ pump.

The plasma membrane potential of human neutrophils was monitored using the anionic dye oxonol-V. The cells maintain a potential of -75 +/- 17 mV when suspended in physiological saline solutions. The cells are scarcely depolarized by extracellular K+ and the depolarization induced by the chemotactic peptide fMet-Leu-Phe is of similar magnitude for cells suspended in 5 or 155 mM K+. Neutrophils are, however, depolarized by suspension in K+-free media or after treatment with ouabain. Neutrophils catalyse Na+-H+ exchange and possess other electroneutral ion transport systems. We propose that the neutrophil membrane potential is generated by an electrogenic Na+ pump, that osmotic stability is achieved by electroneutral ion transport systems and that electrical stability is maintained by anion leakage. Similar mechanisms may also operate in other biological membranes.

Animals↗