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PubMed1984

Mechanism of proline transport in Escherichia coli K12. I. Effect of a membrane potential on the kinetics of 2H+/proline symport in cytoplasmic membrane vesicles.

The stoichiometric coupling mechanism of the membrane potential (delta psi) in the reaction of H+/proline symport was investigated kinetically, using cytoplasmic membrane vesicles of the proline carrier-overproducing strain of Escherichia coli MinS/ pLC4 -45. When a delta psi was imposed across the cytoplasmic membrane by respiration, the Michaelis constant of transport (Kt) was lowered to about 1 microM, which was 2 orders of magnitude smaller than that of passive influx and efflux, and the maximum velocity (Vmax) was concomitantly enhanced as an exponential function of delta psi. Thermodynamically, the carrier translocated proline with a stoichiometry of 2 mol of protons versus 1 mol of substrate when driven by a delta psi at pH 8.0. Data on the delta psi dependence of Vmax of proline transport could be explained quantitatively by the Geck-Heinz hypothesis (Geck, P., and Heinz, E. (1976) Biochim, Biophys. Acta 443, 49-63). A symmetrical model of the 2H+/proline symport via formation of a carrier/H+/substrate (CH+H+S) intermediate is proposed. In this model, the effect of delta psi on the Kt was resolved as stimulation of formation of a transport intermediate, whereas the effect of delta psi on the Vmax was explained by enhancement of translocation of loaded carriers between the two sides of the membrane.

Biological Transport↗
PubMedDate not supplied

Defective function of membrane potential (psi) on sperm of infertile men.

Membrane potential across the plasma membrane (psi) of human sperm was determined by measuring the accumulation of triphenylmethylphosphonium (TPMP+). Washed sperm of fertile or infertile men were suspended, incubated in low-K+ and high-Na+ or high-K+ and low-Na+ medium, and allowed to take up the cation TPMP+ to a steady state (20 min at 37 degrees C). Under these conditions a psi of -75 +/- 6 mV was observed in sperm cells of fertile men, while in spermatozoa of idiopathic and asthenozoospermic infertile men, the psi was of 35 +/- 5 mV and 32 +/- 5 mV, respectively. Upon depolarization of the sperm membrane by K+, the transport system Na(+)-K+ in spermatozoa of idiopathic infertile men decreased 53 +/- 3.5%, while that in sperm cells asthenozoospermic men decreased 57 +/- 3% with respect to spermatozoa of fertile men. The results of these studies indicate their possible application to the diagnosis of male infertility.

Humans↗
PubMed1981

[Membrane potential of Pseudomonas aeruginosa spheroplasts having a cyanide-resistant respiration].

The membrane potential (delta psi) of Ps. aeruginosa spheroplasts was measured by a hydrophobic cation--tetraphenylphosphonium (TPP+) under conditions of simultaneous and separate action of the main respiratory chain and cyanide-resistant oxidase. In all cases, oxidation of endogenous substrates by spheroplasts was followed by generation of a membrane potential of the value of 127--156 mv. An addition of 1 mM cyanide did not practically affect the potential value. The discharge of the potential was attained by further addition of dicyclohexylcarbodiimide (DCCD) or valinomycin. The oxidation of the substrates added by the main respiratory chain was accompanied by an additional increase in the potential by 20--30 mv. In this case, an addition of cyanide decreased the potential by the same value. Oxidation of all substrates, except for TMPD+ ascorbate under conditions of functioning of cyanide-resistant oxidase also increased the potential by 15--50 mv. However, in this case cyanide did not practically affect the increase of the potential. The gain in the potential under TMPD + ascorbate oxidation by cyanide-resistant spheroplasts is prevented by cyanide. A question is discussed as to whether the transfer of reducing equivalents directly via cyanide-resistant oxidase is associated with the generation of a membrane potential or its functioning is not connected with the accumulation of energy in the form available for the cell.

Cyanides↗
PubMed2006

Neuroprotective effect of propofol on necrosis and apoptosis following oxygen-glucose deprivation--relationship between mitochondrial membrane potential and mode of death.

Mitochondrial membrane potential (MMP) appears to play an important role in apoptotic cascade and has been proposed as an index for apoptosis or necrosis. We examined the neuroprotective effect of propofol on mode of death, focusing on MMP. Hippocampal cell culture was divided into three groups: control, oxygen-glucose deprivation for 30 min (30OGD), 90 min (90OGD). Propofol was added to each culture group at a concentration of 0 microM (Vehicle), 0.1 microM (Pro0.1) or 1.0 microM (Pro1.0). MMP was expressed as normalized JC-1 fluorescence. ATP content was assayed using the luciferin-luciferase reaction. Neuronal viability and appearance of apoptosis were also assessed. ATP content was decreased after OGD (0.276 +/- 0.115 microM/microg (control), 0.172 +/- 0.125 microM/microg (30OGD) and 0.096 +/- 0.092 microM/microg (90OGD)). Propofol did not alter ATP content. MMP was hyperpolarized after 30OGD (1.26 +/- 0.23 (vehicle), 1.29 +/- 0.13 (Pro0.1) and 1.18 +/- 0.06 (Pro1.0)) but was depolarized after 90OGD (0.77 +/- 0.04 (vehicle), 0.89 +/- 0.04 (Pro0.1), but Pro1.0 prevented depolarization (1.03 +/- 0.15 (P < 0.05)). Viability of cells significantly decreased to 50.3 +/- 5.7% (vehicle), 46.1 +/- 7.5% (Pro0.1), but Pro1.0 significantly salvaged neurons 65.1 +/- 6.2% (higher than vehicle and Pro0.1 value, P < 0.05) after 90OGD. At 24 h after OGD, TUNEL-positive cells were increased to 34.5 +/- 6.2% (vehicle), 26.7 +/- 7.9% (Pro0.1) and 30.4 +/- 7.1% (Pro1.0) in the 30OGD group. No pharmacological effect of propofol on the incidence of apoptosis was found. Propofol inhibited acute neuronal death accompanied with the maintenance of MMP but did not prevent subsequent apoptosis. Propofol induces a moratorium on neuronal death, during which pharmacological intervention might be able to prevent cell death.

Analysis of Variance↗
PubMed1997

Human red blood cell membrane potential and fluidity in glucose solutions.

This study aimed to investigate the membrane potential and fluidity changes of human red blood cells subjected to isotonic glucose solutions. For the control erythrocytes a membrane potential value of -10.1 +/- 1.8 mV was obtained, whereas erythrocyte membranes in diabetic cells were hyperpolarized, with a potential of -13.9 +/- 2.3 mV. Incubation of both types of red blood cells with increasing glucose concentrations resulted in a substantial hyperpolarization of the cell membranes. Glucose solutions in water had a much stronger effect on membrane potential than glucose dissolved in phosphate-buffered saline. Red blood cell membrane fluidity measurements using the fluorescent label TMADPH did not reveal any significant changes upon incubation with glucose.

Benzothiazoles↗
PubMed1977

Oscillations of membrane potential in L cells. I. Basic characteristics.

The membrane potentials and resistances of L cells were measured using a standard electrophysiological technique. The values obtained in physiological media were around--15 mV and 37Momega, respectively. Almost all the large nondividing L cells (giant L cells) showed spontaneous oscillations of the membrane potential between around -15 and -40 mV. Application of an appropriate electrical or mechanical stimulus was also capable of eliciting responses but such were usually induced only once. The total membrane conductance increased significantly and in parallel with such a hyperpolarizing response. Cooling of the cells and application of metabolic inhibitors to the cells completely blocked the spontaneous oscillation despite the fact that the electrically induced hyperpolarizing response remained. Intracellular K+, Na+ and Cl- concentrations were measured by means of a flame photometer and a chloridometer, and the equilibrium potential for each ion was estimated.

Acetylcholine↗
PubMed1975

Pancreatic acinar cells: ionic dependence of acetylcholine-induced membrane potential and resistance change.

1. Intracellular recordings of membrane potential, input resistance and time constant have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes. The acinar cells were stimulated by acetylcholine (ACh). In some cases ACh was simply directly added to the tissue superfusion bath, in other experiments ACh was applied locally to pancreatic acini by micro-iontophoresis. 2. Current-voltage relations were investigated by injecting rectangular de- or hyperpolarizing current pulses through the recording micro-electrode. Within a relatively wide range (-20 to -70 mV) there was a linear relation between injected current and change in membrane potential. The slope of such linear curves corresponded to an input resistance of about 3-8 M omega. The membrane time constant was about 5-10 msec. 3. ACh depolarized the cell membrane and caused a marked reduction of input resistance and time constant. The minimum latency of the ACh-induced depolarization (microiontophoretic application) was 100-300 msec. Maximal depolarization was about 20 mV. The effect of this local ACh application was abolished by atropine (1-4 x 10-6 M). The blocking effect of atropine was fully reversible. 4. Stimulating with ACh during the passage of large depolarizing current pulses made it possible simultaneously to observe the effect of ACh at two different levels of resting potential (RP). At the spontaneous RP of about minus 40 mV ACh evoked a depolarization of usual magnitude (15-20 mV) while at the artificially displaced level of about -10 mV a small hyperpolarization (about 5 mV) was observed. It therefore appears that the reversal potential of the transmitter equilibrium potential is about -20 mV. 5. Replacement of the superfusion fluid C1 by sulphate or methylsulphate caused an initial short-lasting depolarization, thereafter the normal resting potential was reassumed...

Acetylcholine↗
PubMed2002

Two-state membrane potential transitions of striatal spiny neurons as evidenced by numerical simulations and electrophysiological recordings in awake monkeys.

Spontaneous membrane potential fluctuations of striatal spiny projection neurons play a crucial role in their spike generation. Previous intracellular recording studies in anesthetized rats have shown that the membrane potential of striatal spiny neurons shifts between the depolarized "up" state and the hyperpolarized "down" state. Here we report evidence for the occurrence of such two-state membrane potential transitions by numerical simulations and electrophysiological recordings in awake monkeys. Data from our simulations of a striatal spiny neuron model demonstrated that spike latency histograms of the model neuron displayed two separate (i.e., early and late) peaks in response to excitatory cortical input, corresponding to neuronal activity in the up or down state, respectively. Then, we addressed experimentally whether the latency distribution of cortically induced spike firing of striatal spiny neurons might show dual peaks. Striatal neuron activity was extracellularly recorded in response to electrical stimulation in the two cortical motor-related areas, the primary motor cortex and the supplementary motor area, of awake monkeys. Analysis of spike latency histograms has defined that striatal spiny neurons typically exhibit two temporally distinct peaks, as obtained by the numerical simulations. Thus, the membrane potential shifts between the up and down states appear to occur in striatal spiny neurons of the behaving animal.

Animals↗
PubMedDate not supplied

[Role of phospholipids in the generation of membrane potentials by proteoliposomes].

Closed protein-phospholipid particles (proteoliposomes), obtained by self-assembly method, are capable to generate and to maintain the membrane potential in the case if their protein complex is represented by: a) a complex of mitochondrial ATPase; b) a complex of cytochrome oxidase and cytochrome c and c) bacteriorhodopsin from Halobacterium halobium; and their phospholipid component is represented by phosphatidylethanolamine or by a mixture of mitochondrial phospholipids. Only cytochromoxidase and bacteriorhodopsin (but not ATPase) proteoliposomes with phosphatidylserine are active. Cardiolipin also is not active in experiments with ATPase. Phosphatidylcholine produces in all the cases proteoliposomes incapable of maintaining the membrane potential. It is concluded that the inefficiency of phosphatidylcholine in the formation of proteoliposomes, generating the membrane potential, is due to the impossibility of obtaining closed membrane forms with a high electric resistance. The inefficiency of phosphatidylserine and cardiolipine, in the case of ATPase protein component of proteoliposomes, may be due to a specific requirement of this generator of the membrane potential in phosphatidylethanolamine.

Adenosine Triphosphatases↗
PubMed2005

K+ currents regulate the resting membrane potential, proliferation, and contractile responses in ventricular fibroblasts and myofibroblasts.

Despite the important roles played by ventricular fibroblasts and myofibroblasts in the formation and maintenance of the extracellular matrix, neither the ionic basis for membrane potential nor the effect of modulating membrane potential on function has been analyzed in detail. In this study, whole cell patch-clamp experiments were done using ventricular fibroblasts and myofibroblasts. Time- and voltage-dependent outward K(+) currents were recorded at depolarized potentials, and an inwardly rectifying K(+) (Kir) current was recorded near the resting membrane potential (RMP) and at more hyperpolarized potentials. The apparent reversal potential of Kir currents shifted to more positive potentials as the external K(+) concentration ([K(+)](o)) was raised, and this Kir current was blocked by 100-300 muM Ba(2+). RT-PCR measurements showed that mRNA for Kir2.1 was expressed. Accordingly, we conclude that Kir current is a primary determinant of RMP in both fibroblasts and myofibroblasts. Changes in [K(+)](o) influenced fibroblast membrane potential as well as proliferation and contractile functions. Recordings made with a voltage-sensitive dye, DiBAC(3)(4), showed that 1.5 mM [K(+)](o) resulted in a hyperpolarization, whereas 20 mM [K(+)](o) produced a depolarization. Low [K(+)](o) (1.5 mM) enhanced myofibroblast number relative to control (5.4 mM [K(+)](o)). In contrast, 20 mM [K(+)](o) resulted in a significant reduction in myofibroblast number. In separate assays, 20 mM [K(+)](o) significantly enhanced contraction of collagen I gels seeded with myofibroblasts compared with control mechanical activity in 5.4 mM [K(+)](o). In combination, these results show that ventricular fibroblasts and myofibroblasts express a variety of K(+) channel alpha-subunits and demonstrate that Kir current can modulate RMP and alter essential physiological functions.

Animals↗
PubMed1975

Measurement of membrane potential and estimation of effective fixed-charge density in membranes.

Electrical potentials Em arising across cross-linked phenolsulfonate membrane separating NaCl solutions of molality M1 and M2 have been measured at 25 degrees C. These values of Em have been used in the Nernst equation to calculate values for the apparent transport number ti(app) for the counterion or the co-ion in the membrane. Values of ti(app) together with the limiting value for the cation transport number in the aqueous phase have been used in the equation developed by Kobatake and co-workers to evaluate the membrane permselectivity Ps as a function of external electrolyte concentration. With the help of the equation relating Ps to phiX, the effective fixed-charge density in the membrane (where phi is a constant, 0 less than phi less than 1, and X is the membrane stochiometric charge density and can be evaluated by chemical analysis of the membrane phase), values for phiX and phi have been determined. Values of phi were low in dilute solutions and increased with increase in the concentration of the external solution. Similar behavior was noted in the case of another membrane system, cross-linked polymethacrylic acid in contact with KOH solutions. On the other hand, the membrane system, "untreated" collodion in contact with KCl solutions, exhibited a behavior in which the values of phi, low in dilute solutions, increased and then decreased following a gradual increase in the external concentration. This slight divergence in its behavior was attributed to the heterogeneity of the collodion membrane structure. The reliability of this potentiometric method to estimate effective fixed-charge density in membranes has been discussed in relation to a similar but old method due to Teorell, Meyer and Sievers. Also the significance of the values derived for phi has been pointed out.

Evaluation Studies as Topic↗
PubMedDate not supplied

[Dynamics of membrane potential of limb muscular tissue in acute hypoxia induced by blood loss].

The authors studied the frequency dependence of the membrane potential of the rat quadriceps femoris muscle fibres in acute hypoxia caused by blood loss on its severity and duration. The membrane potential reduced with the gradual development of metabolic disorders in the tissue. Approximation revealed an exponential character of the dependence of the cell membrane potential on the severity and duration of hypoxia. The severity of the hypoxic disorders in the tissue can be judged from the value of the membrane potential.

Animals↗
PubMed1984

Voltage clamp studies of fertilization in sea urchin eggs. I. Effect of clamped membrane potential on sperm entry, activation, and development.

To analyze the role of the activation potential (a positive shift of the membrane potential which occurs following sperm attachment) in fertilization and development of the sea urchin egg, unfertilized Lytechinus variegatus eggs were voltage clamped at membrane potentials (Em) from +20 to -90 mV, and then inseminated. Either a fast two electrode voltage clamp, or a single electrode switched voltage clamp was used. The clamp was maintained for 3 to 15 min after initiation of a conductance increase. At Em more positive than +18 mV, even though many sperm may attach, the egg remains completely inert (Jaffe, Nature (London) 261, 68-71, 1976). At Em from +17 to -90 mV, all inseminated eggs elevate normal fertilization envelopes, although substantially increased concentrations of sperm are required at Em from +17 to +12 mV. Whether cleavage occurs depends on the clamped Em. When clamped at Em from +17 to -25 mV, 100% of activated eggs cleave. However, when clamped at Em from -26 to -75 mV the percentage of activated eggs which cleave progressively decreases. At clamped Em between -76 and -90 mV, none of the activated eggs cleave. All monospermic voltage clamped eggs that cleave develop to normal swimming blastulae. In all eggs that fail to cleave (clamped at Em more negative than -30 mV), sperm penetration is blocked, the sperm is lifted off the egg surface as the fertilization envelope rises, and a sperm aster never forms. Preventing formation of the fertilization envelope by prior disruption of the vitelline layer with dithiothreitol does not promote entry of the sperm. In conclusion, preventing the depolarization normally associated with fertilization suppresses sperm entry in the sea urchin egg, yet activation proceeds. Present evidence suggests an effect of the electrical field across the plasma membrane in suppressing sperm entry.

Action Potentials↗
PubMedDate not supplied

Energy substrates, mitochondrial membrane potential and human preimplantation embryo division.

Carbohydrate additives to modern embryo culture media are based on three basic energy sources, glucose, pyruvate and lactate. Although the use of these substrates is almost universal, debate continues as to the roles of the individual components in the human. This is mainly due to the lack of human embryos for research and the reliance on animal model systems. In the present work, the human embryo was used to study the role of the above simple substrates in the maintenance of the mitochondrial membrane potential and cell division. The mitochondrial membrane potential was measured with fluorescence techniques. Cell division was scored as the number of blastomeres on day 3. Both the mitochondrial membrane potential and cell division were dramatically lost in the absence of energy sources. The mitochondrial membrane potential and cell division were normal in media containing all three energy sources, or in pyruvate-containing media. Both glucose and lactate individually proved poor energy sources for the maintenance of the mitochondrial membrane potential. However, cell division continued in the presence of glucose, suggesting that some energy production can continue. These data suggest that pyruvate is an absolute requirement for mitochondrial respiration and cell cleavage during human preimplantation development. The role of lactate is as yet unclear.

Adult↗
PubMed1996

Continuous monitoring of mitochondrial membrane potential in hepatocyte cell suspensions.

We report a simple fluorometric method for the continuous monitoring of mitochondrial membrane potential and cell viability in suspensions of hepatocytes exposed in vitro to cytotoxic agents. Suspensions of freshly isolated hepatocytes (10(6) cells/mL) preloaded with rhodamine 123 (Rh 123, 100 mumol/L) are transferred to a thermostatically controlled mixed cuvette to which the desired cytotoxic agent is added. Rh 123 is a cationic fluorophore that is actively accumulated by cells in direct proportion to the mitochondrial membrane potential. Cell viability was estimated by monitoring propidium iodide (PI) fluorescence. Exposure of cell suspensions to the mitochondrial uncoupling agent FCCP caused an immediate and titratable increase in Rh 123 fluorescence. Subsequent treatment with digitonin did not change Rh 123 fluorescence, suggeseting that Rh 123 equilibrates rapidly across the intact cell membrane. Likewise, treatment of hepatocyte suspensions with inhibitors of mitochondrial respiration (rotenone, cyanide, or menadione) caused an immediate increase in Rh 123 fluorescence. This was accompanied by a progressive increase in PI fluorescence, suggesting a causal relationship between mitochondrial depolarization and cell injury. In contrast, 1,4-benzoquinone caused a time-dependent and linear increase in PI fluorescence that paralleled changes in Rh 123 fluorescence. Comparing the time courses for changes in PI and Rh 123 fluorescence suggests that for benzoquinone, the depolarization of the mitochondria is a consequence rather than a cause of the cell injury. This modified procedure provides a simple and specific technique for continuously monitoring mitochondrial membrane potential and cell viability in suspensions of freshly isolated hepatocytes. The advantage is that there is no need to separate cells from the incubation medium, making it possible to record real-time changes in mitochondrial membrane potential and cell viability throughout the in vitro exposure period.

Animals↗
PubMed2002

Intracellular QX-314 causes depression of membrane potential oscillations in lamprey spinal neurons during fictive locomotion.

Spinal neurons undergo large cyclic membrane potential oscillations during fictive locomotion in lamprey. It was investigated whether these oscillations were due only to synaptically driven excitatory and inhibitory potentials or if voltage-dependent inward conductances also contribute to the depolarizing phase by using N-(2,6-dimethylphenyl carbamoylmethyl)triethylammonium bromide (QX-314) administered intracellularly during fictive locomotion. QX-314 intracellularly blocks inactivating and persistent Na+ channels, and in some neurons, effects on certain other types of channels have been reported. To detail the effects of QX-314 on Na+ and Ca2+ channels, we used dissociated lamprey neurons recorded under whole cell voltage clamp. At low intracellular concentrations of QX-314 (0.2 mM), inactivating Na+ channels were blocked and no effects were exerted on Ca2+ channels (also at 0.5 mM). At 10 mM QX-314, there was, however a marked reduction of I(Ca). In the isolated spinal cord of the lamprey, fictive locomotion was induced by superfusing the spinal cord with Ringer's solution containing N-methyl-D-aspartate (NMDA), while recording the locomotor activity from the ventral roots. Simultaneously, identified spinal neurons were recorded intracellularly, while infusing QX-314 from the microelectrode. Patch electrodes cannot be used in the intact spinal cord, and therefore "sharp" electrodes were used. The amplitude of the oscillations was consistently reduced by 20-25% in motoneurons (P < 0.05) and unidentified spinal neurons (P < 0.005). The onset of the effect started a few minutes after impalement and reached a stable level within 30 min. These effects thus show that QX-314 causes a reduction in the amplitude of membrane potential oscillations during fictive locomotion. We also investigated whether QX-314 could affect glutamate currents by applying short pulses of glutamate from an extracellular pipette. No changes were observed. We also found no evidence for a persistent Na+ current in dissociated neurons, but these cells have a much-reduced dendritic tree. The results indicate that there is an inward conductance, which is sensitive to QX-314, during membrane potential oscillations that "boosts" the synaptic drive during fictive locomotion. Taken together, the results suggest that inactivating Na+ channels contribute to this inward conductance although persistent Na+ channels, if present on dendrites, could possibly also contribute to shaping the membrane potential oscillations.

Action Potentials↗
PubMed1985

The use of 36Cl- to measure cell plasma membrane potential in isolated hepatocytes--effects of cyclic AMP and bicarbonate ions.

The plasma membrane potential of hepatocytes was calculated from the distribution of 36Cl-. The potential observed under several conditions was equivalent to that previously measured using microelectrodes in perfused liver. Dibutyryl cAMP increased the membrane potential. Replacement of bicarbonate ions by morpholinosulphonate decreased the potential and reduced the effect of cAMP. The effect of both bicarbonate and cAMP was abolished by ouabain. Both bicarbonate and cAMP stimulated the activity of the (Na+ + K+)-ATPase as measured by ouabain-inhibitable 86Rb+ uptake. It is suggested that the stimulation of alanine transport by these effectors is mediated by an increase in cell membrane potential via stimulation of the (Na+ + K+)-ATPase.

Alanine↗
PubMed2000

The role of membrane potential and calcium kinetic changes in the pathogenesis of vascular hyporeactivity during severe shock.

OBJECTIVE: To determine the role of membrane potential and intracellular calcium kinetic changes in producing vascular hyporeactivity during severe hemorrhagic shock. METHODS: Rats were subjected to hemorrhagic shock (HS) for 2 hours. The spinotrapezius muscle was prepared for microscopy and the responses of arterioles in the muscle to norepinephrine (NE) were tested. The resting membrane potentials of isolated arterial strips were measured with a microelectrode. Membrane potential and intracellular Ca2+ ([Ca2+]i) changes in isolated arteriolar smooth muscle cells (ASMCs) were determined with fluorescent probes and a confocal microscopy. RESULTS: The arteriolar resting membrane potential was decreased from -36.7 +/- 6.3 mV in control to -29.2 +/- 5.3 mV concurrent with the increase of vasoreactivity to NE at 20 minutes after HS. At 120 minutes post-HS, the resting potential hyperpolarized to -51.9 +/- 9.1 mV, and NE stimulated [Ca2+]i increase was reduced to 50% of the control values during the appearance of arteriolar hyporeactivity, i.e. the NE threshold of the arteriolar response increased 15 fold 2 hours after the onset of hemorrhage as compared with normal animals. The state of vasoreactivity was closely related to the resting potential of vascular smooth muscle in hemorrhagic shock, with a correlation coefficient of 0.96. Treatment with glybenclamide, a selective blocker of ATP-sensitive K+ (KATP) channels, decreased the resting potential, increased NE-stimulated [Ca2+]i increase, and partially restored vasoreactivity in severe hemorrhagic shock. CONCLUSION: The results suggested that membrane hyperpolarization and the reduction of NE-stimulated [Ca2+]i increase in smooth muscle cells appeared to contribute to the vascular hyporeactivity in hemorrhagic shock. The mechanism is likely to involve in KATP channels.

Animals↗