Spontaneous transient outward currents and delayed rectifier K+ current: effects of hypoxia

1998 ◽  
Vol 275 (1) ◽  
pp. L145-L154 ◽  
Author(s):  
C. Vandier ◽  
M. Delpech ◽  
P. Bonnet
Keyword(s):  
Steady State ◽  
Outward Current ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Outward Currents ◽  
K Current ◽  
The Mean ◽  
Patch Configuration ◽  
Spontaneous Transient Outward Currents ◽  
Dependent Mechanism

Single smooth muscle cells of rabbit intrapulmonary artery were voltage clamped using the perforated-patch configuration of the patch-clamp technique. We observed spontaneous transient outward currents (STOCs) and a steady-state outward current. Because STOCs were tetraethylammonium sensitive and activated by Ca2+ influx, they were believed to represent activation of Ca2+-activated K+ channels. The steady-state outward current, which was sensitive to 4-aminopyridine, was the delayed rectifier K+ current. In cells voltage clamped at 0 mV, we found that STOCs were not randomly distributed in amplitude but were composed of multiples of 1.57 ± 0.56 pA/pF. The mean frequency of STOCs was 5.51 ± 3.49 Hz. Ryanodine (10 μM), caffeine (5 mM), thapsigargin (200 nM), and hypoxia [Formula: see text] = 10 mmHg) decreased STOCs. The effect of hypoxia on STOCs was partially reversible only if the experiment was conducted in the presence of thapsigargin. Hypoxia and thapsigargin decrease steady-state outward current. Thapsigargin and removal of external Ca2+abolished the effect of hypoxia, suggesting that hypoxia decreases steady-state outward current by a Ca2+-dependent mechanism.

Ca-Induced K+-Outward Current in Paramecium Tetraurelia

1980 ◽  
Vol 88 (1) ◽  
pp. 293-304 ◽  
Author(s):  
YOUKO SATOW ◽  
CHING KUNG
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Outward Current ◽  
Paramecium Tetraurelia ◽  
Ca Channels ◽  
Outward Currents ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
K Current ◽  
K Outward Current

Late K-outward currents upon membrane depolarization were recorded in Paramecium tetraurelia under a voltage clamp. A Ca-induced K-outward component is demonstrated by subtracting the value of the outward current in a pawn A mutant lacking functional Ca-channels (pwA500). The Ca-induced K-outward current activates slowly, reaching a peak after 100 to 1000 ms. The current then remains steady or reaches the steady state after a decline of several seconds. EGTA2- injection experiments show that the Ca-induced K-outward current is dependent on the internal Ca2+ concentration. The current is shown to depend on the voltage-dependent Ca conductance, by study of the leaky pawn A mutant (pwA132), which has a lowered Ca conductance as well as a lowered Ca-induced K-current. The Ca-induced GK is thus indirectly dependent on the voltage. The maximal GK is about 40 nmho/cell at + 7 mV in 4 mM-K+. The Ca-induced K current is sustained throughout the prolonged depolarization and the prolonged ciliary reversal.

Transient potassium currents in avian sensory neurons

1990 ◽  
Vol 63 (4) ◽  
pp. 725-737 ◽  
Author(s):  
S. K. Florio ◽  
C. D. Westbrook ◽  
M. R. Vasko ◽  
R. J. Bauer ◽  
J. L. Kenyon
Keyword(s):  
Single Channel ◽  
Outward Current ◽  
Potassium Currents ◽  
Delayed Rectifier ◽  
Transient Outward Current ◽  
Single Channels ◽  
Patch Clamp Technique ◽  
Small Component ◽  
Whole Cell ◽  
Outward Currents

1. We used the patch-clamp technique to study voltage-activated transient potassium currents in freshly dispersed and cultured chick dorsal root ganglion (DRG) cells. Whole-cell and cell-attached patch currents were recorded under conditions appropriate for recording potassium currents. 2. In whole-cell experiments, 100-ms depolarizations from normal resting potentials (-50 to -70 mV) elicited sustained outward currents that inactivated over a time scale of seconds. We attribute this behavior to a component of delayed rectifier current. After conditioning hyperpolarizations to potentials negative to -80 mV, depolarizations elicited transient outward current components that inactivated with time constants in the range of 8-26 ms. We attribute this behavior to a transient outward current component. 3. Conditioning hyperpolarizations increased the rate of activation of the net outward current implying that the removal of inactivation of the transient outward current allows it to contribute to early outward current during depolarizations from negative potentials. 4. Transient current was more prominent on the day the cells were dispersed and decreased with time in culture. 5. In cell-attached patches, single channels mediating outward currents were observed that were inactive at resting potentials but were active transiently during depolarizations to potentials positive to -30 mV. The probability of channels being open increased rapidly (peaking within approximately 6 ms) and then declined with a time constant in the range of 13-30 ms. With sodium as the main extracellular cation, single-channel conductances ranged from 18 to 32 pS. With potassium as the main extracellular cation, the single-channel conductance was approximately 43 pS, and the channel current reversed near 0 mV, as expected for a potassium current. 6. We conclude that the transient potassium channels mediate the component of transient outward current seen in the whole-cell experiments. This current is a relatively small component of the net current during depolarizations from normal resting potentials, but it can contribute significant outward current early in depolarizations from hyperpolarized potentials.

scholarly journals Voltage-dependent conductances in Limulus ventral photoreceptors.

1982 ◽  
Vol 79 (2) ◽  
pp. 187-209 ◽  
Author(s):  
J E Lisman ◽  
G L Fain ◽  
P M O'Day
Keyword(s):  
Outward Current ◽  
Delayed Rectifier ◽  
Molluscan Neurons ◽  
Inward Current ◽  
Transient Component ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
A Current

The voltage-dependent conductances of Limulus ventral photoreceptors have been investigated using a voltage-clamp technique. Depolarization in the dark induces inward and outward currents. The inward current is reduced by removing Na+ or Ca2+ and is abolished by removing both ions. These results suggest that both Na+ and Ca2+ carry voltage-dependent inward current. Inward current is insensitive to tetrodotoxin but is blocked by external Ni2+. The outward current has a large transient component that is followed by a smaller maintained component. Intracellular tetraethylammonium preferentially reduces the maintained component, and extracellular 4-amino pyridine preferentially reduces the transient component. Neither component is strongly affected by removal of extracellular Ca2+ or by intracellular injection of EGTA. It is concluded that the photoreceptors contain at least three separate voltage-dependent conductances: 1) a conductance giving rise to inward currents; 2) a delayed rectifier giving rise to maintained outward K+ current; and 3) a rapidly inactivating K+ conductance similar to the A current of molluscan neurons.

Characterization of macroscopic outward currents of canine colonic myocytes

1989 ◽  
Vol 257 (3) ◽  
pp. C461-C469 ◽  
Author(s):  
W. C. Cole ◽  
K. M. Sanders
Keyword(s):  
Outward Current ◽  
Cell Voltage ◽  
Muscle Cells ◽  
Time Dependent ◽  
Delayed Rectifier ◽  
Delayed Rectifier Current ◽  
Outward Currents ◽  
Voltage Dependent ◽  
K Current ◽  
Time Courses

Outward currents of colonic smooth muscle cells were characterized by the whole cell voltage-clamp method. Four components of outward current were identified: a time-independent and three time-dependent components. The time-dependent current showed strong outward rectification positive to -25 mV and was blocked by tetraethylammonium. The time-dependent components were separated on the basis of their time courses, voltage dependence, and pharmacological sensitivities. They are as follows. 1) A Ca2+-activated K current sensitive to external Ca2+ and Ca2+ influx was blocked by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (0.1 X 10(-3) M) and nifedipine (1 X 10(-6) and was increased by elevated Ca2+ (8 X 10(-6) M) and BAY K 8644 (1 X 10(-6) M). 2) A "delayed rectifier" current was observed that decayed slowly with time and showed no voltage-dependent inactivation. 3) Spontaneous transient outward currents that were blocked by ryanodine (2 X 10(-6) M) were also recorded. The possible contributions of these currents to the electrical activity of colonic muscle cells in situ are discussed. Ca2+-activated K current may contribute a significant conductance to the repolarizing phase of electrical slow waves.

An outwardly rectifying K+ current active near resting potential in human retinal pigment epithelial cells

1995 ◽  
Vol 269 (1) ◽  
pp. C179-C187 ◽  
Author(s):  
B. A. Hughes ◽  
M. Takahira ◽  
Y. Segawa
Keyword(s):  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Outward Current ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Rpe Cells ◽  
Pigment Epithelial ◽  
K Current

Currents in freshly dissociated adult human retinal pigment epithelial (RPE) cells were studied using the perforated patch-clamp technique. The zero-current potential (V0) averaged -48.9 +/- 7.7 mV (n = 50). Depolarizing voltage pulses from -70 mV evoked an outward current that activated with first-order kinetics and that did not inactivate during prolonged depolarizations. Repolarizing the membrane potential produced tail currents that reversed near the K+ equilibrium potential, indicating that the sustained outward current was carried mainly by K+. The outwardly rectifying K+ conductance (gK) had an activation threshold voltage near -60 mV and was half-maximal at -37 mV. Approximately 25% of gK was active at the average V0. The K+ current was nearly completely blocked by 2 mM Ba2+ but was relatively insensitive to 20 mM tetraethylammonium. The kinetics, voltage dependence, and blocker sensitivity of this current clearly distinguish it from delayed rectifier K+ currents previously identified in RPE cells. We conclude that the sustained outward K+ current may help establish the resting potential of the apical and/or basolateral membranes and may also participate in K+ transport across the RPE.

Permeability of time-dependent K+ channel in guinea pig ventricular myocytes to Cs+, Na+, NH4+, and Rb+

1990 ◽  
Vol 259 (5) ◽  
pp. H1448-H1454 ◽  
Author(s):  
R. W. Hadley ◽  
J. R. Hume
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Outward Current ◽  
Time Dependent ◽  
K Channel ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Outward Currents

Currents through time-dependent K+ channels (also referred to as IK or the delayed rectifier) were studied with the whole cell patch-clamp technique in isolated guinea pig ventricular myocytes. IK measurements were restricted to the examination of deactivation tail currents. Substitution of various monovalent cations for external K+ produced shifts of the reversal potential of IK. These shifts were used to calculate permeability ratios relative to K+. The permeability sequence for the IK channels was K+ = Rb+ greater than NH4+ = Cs+ greater than Na+. Time-dependent outward currents were also examined when the myocytes were dialyzed with Cs+ instead of K+. A sizeable time-dependent outward current, quite similar to that seen with K+ dialysis, was demonstrated. This current was primarily carried by intracellular Cs+, as the reversal potential of the current shifted 46 mV per 10-fold change of external Cs+ concentration. The significance of Cs+ permeation through IK channels is discussed with respect to the common use of Cs+ in isolating other currents.

Choline chloride activates time-dependent and time-independent K+ currents in dog atrial myocytes

1994 ◽  
Vol 266 (1) ◽  
pp. C42-C51 ◽  
Author(s):  
B. Fermini ◽  
S. Nattel
Keyword(s):  
Choline Chloride ◽  
Outward Current ◽  
Time Dependent ◽  
Equilibrium Potential ◽  
Delayed Rectifier ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Voltage Dependent ◽  
K Current ◽  
K Currents

Using the whole cell configuration of the patch-clamp technique, we studied the effect of isotonic replacement of bath sodium chloride (NaCl) by choline chloride (ChCl) in dog atrial myocytes. Our results show that ChCl triggered 1) activation of a time-independent background current, characterized by a shift of the holding current in the outward direction at potentials positive to the K+ equilibrium potential (EK), and 2) activation of a time- and voltage-dependent outward current, following depolarizing voltage steps positive to EK. Because the choline-induced current obtained by depolarizing steps exhibited properties similar to the delayed rectifier K+ current (IK), we named it IKCh. The amplitude of IKCh was determined by extracellular ChCl concentration, and this current was generally undetectable in the absence of ChCl. IKCh was not activated by acetylcholine (0.001-1.0 mM) or carbachol (10 microM) and could not be recorded in the absence of ChCl or when external NaCl was replaced by sucrose or tetramethylammonium chloride. IKCh was inhibited by atropine (0.01-1.0 microM) but not by the M1 antagonist pirenzepine (up to 10 microM). This current was carried mainly by K+ and was inhibited by CsCl (120 mM, in the pipette) or barium (1 mM, in the bath). We conclude that in dog atrial myocytes, ChCl activates a background conductance comparable to ACh-dependent K+ current, together with a time-dependent K+ current showing properties similar to IK.

Extracellular ATP regulation of feline tracheal submucosal gland secretion

1994 ◽  
Vol 267 (2) ◽  
pp. L159-L164 ◽  
Author(s):  
S. Shimura ◽  
T. Sasaki ◽  
M. Nagaki ◽  
T. Takishima ◽  
K. Shirato
Keyword(s):  
Phosphodiesterase Inhibitor ◽  
Outward Current ◽  
Acinar Cells ◽  
Initial Increase ◽  
Patch Clamp Technique ◽  
Receptor Stimulation ◽  
Outward Currents ◽  
Submucosal Glands ◽  
K Current ◽  
Atp Regulation

The standard patch-clamp technique was employed on enzymatically digested acinar cells of submucosal glands isolated from feline trachea. ATP (-10(-3) M) evoked bidirectional current responses and an initial inward current at -80 mV (Cl- current) was followed by an outward current at 0 mV of membrane potential (K+ current). Isoproterenol (ISO) alone did not evoke any significant current responses. However, ISO augmented the ATP-induced inward and outward currents. A phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, mimicked the augmentation by ISO. [Ca2+]i of acinar cells in isolated gland was measured using a fluorescent dye, fura 2. ATP (-10(-3) M) induced an immediate increase in [Ca2+]i followed by a prolonged plateau, and Ca2+ removal resulted in an initial increase alone without the prolonged phase. ISO also augmented the ATP-evoked increases in [Ca2+]i mainly in the plateau phases. Mucus glycoprotein (MGP) secretion was estimated by measuring trichloroacetic acid-precipitable [3H]glycoconjugates from isolated glands. ATP (-10(-3) M) evoked significant MGP secretion and ISO enhanced the ATP-induced MGP secretion. In contrast, adenosine (-10(-3) M) produced no significant responses in current, MGP secretion, or [Ca2+]i. These findings suggest that 1) P2-receptor stimulation and the resultant [Ca2+]i rise induced both electrolyte and MGP secretions and 2) ATP-induced secretion is enhanced by an adenosine 3',5'-cyclic monophosphate intracellular concentration [cAMP]i-rise after beta-receptor stimulation in airway submucosal glands.

Inhibition of metabolism abolishes transient outward current in rabbit atrial myocytes

1994 ◽  
Vol 266 (1) ◽  
pp. H182-H190 ◽  
Author(s):  
A. Ogbaghebriel ◽  
A. Shrier
Keyword(s):  
Steady State ◽  
Patch Clamp ◽  
Potassium Current ◽  
Outward Current ◽  
Transient Outward Current ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Outward Currents ◽  
Inward Currents ◽  
Inhibition Of Metabolism

Outward currents were measured in single rabbit atrial myocytes using the whole cell configuration of the patch-clamp technique in the presence of tetrodotoxin (5–10 microM) and MnCl2 (2 mM) to block inward currents. Depolarizing voltage-clamp steps from a holding potential of -80 mV elicited a predominant 4-aminopyridine (4-AP)-sensitive transient outward current (Ito). Inhibitors of oxidative metabolism, 2,4-dinitrophenol (DNP; 100 microM) and cyanide (3 mM) abolished Ito and caused a large increase in the steady-state outward current. This steady-state outward current was inhibited by glibenclamide (5 microM), a blocker of the ATP-regulated potassium current (IKATP). In the presence of DNP, glibenclamide (5 microM) not only inhibited IKATP but also partially restored Ito. Absence of ATP from the pipette produced effects on outward currents similar to those induced by DNP or cyanide. We conclude that metabolic inhibition abolishes Ito in rabbit atrial myocytes and suggest that ATP may be required for the activation of the channel.

Voltage-activated whole-cell K+ currents in lamina cells of the desert locust schistocerca gregaria

1999 ◽  
Vol 202 (14) ◽  
pp. 1939-1951 ◽  
Author(s):  
C. Benkenstein ◽  
M. Schmidt ◽  
M. Gewecke
Keyword(s):  
Voltage Dependence ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Group I ◽  
Outward Currents ◽  
K Current ◽  
Group Ii ◽  
I Cells ◽  
In Cells

Voltage-dependent outward currents were studied in freshly dissociated somata of locust lamina cells. These currents were recorded in 142 somata using the whole-cell patch-clamp technique. By measuring the reversal potential at altered external [K+] and by replacing internal K+ with Cs+, we determined that the outward currents were carried by K+. The outward currents consist of a transient A-type K+ current (KA) and a delayed-rectifier-like K+ current (KD). Amongst the cells studied, we observed two distinct groups of cells. The most obvious difference between the two groups is that in group I cells the total outward current is dominated by KA (KA/KD=12.5), whereas in group II cells KA makes a smaller contribution (KA/KD=2.1). Furthermore, in cells of group I, the KA current shows a steeper voltage-dependence of activation, where VG50 is −29.9 mV and s is 11.9 (N=22), and inactivation, where VI50 is −84.5 mV and s is −6.3 (N=18), compared with the KA current in cells of group II: VG50=−7.9 mV; s=26.6 (N=36) and VI50=−68.4 mV; s=−7.5 (N=21) (VG50 is the voltage at which the whole-cell conductance G is half-maximally activated, VI50 is the voltage of half-maximal inactivation and s is the slope of the voltage-dependence). The transient KA current in group I cells decayed mono-exponentially. The decay of the KA current in group II cells was fitted with a double-exponential curve and was significantly faster than in group I cells. In contrast to the large differences in KA currents, the KD currents appeared to be quite similar in the two groups of cells.

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