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Potassium Replacement

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4321. Identification of delayed potassium and calcium currents in the rat sympathetic neurone under voltage clamp. (Full text)

Identification of delayed potassium and calcium currents in the rat sympathetic neurone under voltage clamp. Post-ganglionic neurones of the isolated rat superior cervical ganglion were studied at 37 degrees C under two-electrode voltage-clamp conditions. Membrane depolarization beyond -40 mV from holding levels between -50 and -100 mV produced a delayed outward current which exhibited no inactivation within this voltage range. The current is carried primarily by K+ ions and its instantaneous I (...) -V relation is linear. The total outward current could be separated into two distinct components on the basis of ion-substitution experiments. A voltage-dependent component of the delayed current, termed IK(V), is activated by membrane depolarization beyond -40 mV when Ca2+ fluxes are selectively blocked by Cd2+ or in Ca2+-free solution. IK(V) develops following first-order kinetics and rises to a peak with a voltage-dependent delay (239 ms at -30 mV and 23 ms at +10 mV). GK(V) attains

1985 The Journal of physiology PubMed abstract

4322. Apical membrane potassium and chloride permeabilities in surface cells of rabbit descending colon epithelium. (Full text)

Apical membrane potassium and chloride permeabilities in surface cells of rabbit descending colon epithelium. The apical membranes of surface cells in the rabbit descending colon possess a significant ionic conductance in parallel to amiloride-blockable Na+ channels. The identity of the ion(s) responsible for the amiloride-insensitive conductance is unknown. The purpose of the present paper was to assess the permeability and net driving forces for K+ and Cl- across this membrane using (...) conventional and ion-sensitive micro-electrode techniques. Intracellular Cl- activity (aiCl) averaged 23 +/- 2 mM with an equilibrium potential (ECl) of -38 +/- 2 mV. This value is less than previous estimates of the electromotive force (e.m.f.) of the amiloride-insensitive pathway (ca. -50 mV). Consequently, Cl- alone cannot account for the amiloride-insensitive conductance. Replacement of Cl- by gluconate in the serosal solution decreased aiCl to 17 +/- 2.8 mM. aiCl was lowered to approximately 1 mM

1985 The Journal of physiology PubMed abstract

4323. A voltage-gated potassium channel in human T lymphocytes. (Full text)

A voltage-gated potassium channel in human T lymphocytes. Human peripheral T lymphocytes were studied at 20-24 degrees C using the gigaohm seal recording technique in whole-cell or outside-out patch conformations. The predominant ion channel present under the conditions employed was a voltage-gated K+ channel closely resembling delayed rectifier K+ channels of nerve and muscle. The maximum K+ conductance in ninety T lymphocytes ranged from 0.7 to 8.9 nS, with a mean of 4.2 nS. The estimated (...) permeability. Tail current kinetics were slowed about 2-fold by raising the external K+ concentration from 4.5 to 160 mM, and were 5 times slower in Rb+ Ringer solution than in K+ Ringer solution. Single K+ channel currents had two amplitudes corresponding to about 9 and 16 pS in Ringer solution. Replacing Ringer solution with isotonic K+ Ringer solution increased the unitary conductance and resulted in inward rectification of the unitary current-voltage relation. Comparable effects of external K+ were

1985 The Journal of physiology PubMed abstract

4324. Slow components of potassium tail currents in rat skeletal muscle (Full text)

for the latter did not allow significant outward current. Substitution of Rb for extracellular K abolished current through the anomalous (inward-going) rectifier and at the same time eliminated the slow inward tail, which suggests that the slow inward tail current flows through anomalous rectifier channels. The amplitude of the slow inward tail was increased and VK was shifted in the depolarizing direction by longer conditioning pulses. The shift in VK implies that during outward currents potassium (...) Slow components of potassium tail currents in rat skeletal muscle The kinetics of potassium tail currents have been studied in the omohyoid muscle of the rat using the three-microelectrode voltage-clamp technique. The currents were elicited by a two-pulse protocol in which a conditioning pulse to open channels was followed by a test step to varying levels. The tail currents reversed at a single well-defined potential (VK). At hyperpolarized test potentials (-100 mV and below), tail currents

1983 The Journal of general physiology PubMed abstract

4325. Calcium- and voltage-activated potassium channels in human macrophages. (Full text)

Calcium- and voltage-activated potassium channels in human macrophages. Single calcium-activated potassium channel currents were recorded in intact and excised membrane patches from cultured human macrophages. Channel conductance was 240 pS in symmetrical 145 mM K+ and 130 pS in 5 mM external K+. Lower conductance current fluctuations (40% of the larger channels) with the same reversal potential as the higher conductance channels were noted in some patches. Ion substitution experiments (...) indicated that the channel is permeable to potassium and relatively impermeable to sodium. The frequency of channel opening increased with depolarization and intracellular calcium concentration. At 10(-7) M (Ca++)i, channel activity was evident only at potentials of +40 mV or more depolarized, while at 10(-5) M, channels were open at all voltages tested (-40 to +60 mV). In intact patches, channels were seen at depolarized patch potentials of +50 mV or greater, indicating that the ionized calcium

1984 Biophysical journal PubMed abstract

4326. Acetylcholine-evoked potassium release in the mouse pancreas. (Full text)

- was replaced by bromide (Br-) the response to ACh was virtually unaffected. When sodium (Na+) was replaced by lithium (Li+) ACh did not evoke K+ release but instead K+ uptake was observed. However, when Tris+ was substituted for Na+ ACh evoked a very small K+ release. Pre-treatment of pancreatic segments with 10(-3) M-ouabain resulted in a marked sustained K+ release. In the continuing presence of ouabain ACh induced a further increase in K+ outflow. Pre-treatment of the preparation with 10 mM-tetraethyl (...) Acetylcholine-evoked potassium release in the mouse pancreas. Mouse pancreatic segments were superfused with physiological saline solutions and the K+ concentration in the effluent was measured by flame photometry. Acetylcholine (ACh) evoked a dose-dependent and transient increase in the K+ concentration in the effluent (K+ release). The removal of calcium (Ca2+) from the superfusing solution and addition of 10(-4) M-EGTA (ethyleneglycol-bis-(beta-amino-ethylether)N,N'-tetraacetic acid) caused

1985 The Journal of physiology PubMed abstract

4327. Potassium Transport in Corn Roots : IV. Characterization of the Linear Component (Full text)

Potassium Transport in Corn Roots : IV. Characterization of the Linear Component A detailed examination was conducted on the linear, or first-order kinetic component for K(+)((86)Rb(+)) influx into root segments of both low- and high-salt grown corn seedlings (Zea mays [A632 x Oh 43]). In tissue from both low- and high-salt grown roots, replacement of Cl(-) in the uptake solution by either SO(4) (2-), H(2)PO(4) (-), or NO(3) (-) caused a significant (50-60%) and specific inhibition (...) of the linear component of K(+) influx. The anion transport inhibitor, 4,4'-diisothiocyano-2,2'-disulfonic acid, was found to abolish saturable Cl(-) influx in corn roots while causing a significant (50-60%) and specific inhibition of the linear K(+) uptake system; this inhibition was identical to that observed when Cl(-) was replaced by other anions in the K(+) uptake solution. Additionally, the quaternary ammonium cation, tetraethylammonium, which has been shown to block K(+) channels in nerve axons, also

1985 Plant physiology PubMed abstract

4328. On the mechanism of a pH-induced rise in membrane potassium conductance in hamster eggs. (Full text)

On the mechanism of a pH-induced rise in membrane potassium conductance in hamster eggs. 1. The effect of external pH (pHo) on the membrane potential and resistance of unfertilized zona-free hamster eggs was investigated by intracellular recording techniques. 2. A hyperpolarization of the hamster egg membrane was induced by raising the extracellular pH above 8.0. This hyperpolarization was accompanied by a rise in membrane conductance and was reversible by washing the egg. 3. The estimated (...) value of the reversal potential of the hyperpolarizing response to a solution with pHo 9.5 was about -85 mV. The membrane potential changed linearly with log [K+]o with a slope of 43 +/- 2 mV (mean +/- S.D.; n = 4) for a 10-fold change in [K+]o, while it was unaltered by the removal of Cl- from the solution. 4. The amplitude of the pHo-induced hyperpolarization decreased substantially as [Ca2+]o was lowered from 20 to 1 mM. Sr2+ could substitute for Ca2+ in sustaining the response to high pHo

1988 The Journal of physiology PubMed abstract

4329. Na+-K+ pump activities of high- and low-potassium sheep red cells with internal magnesium and calcium altered by A23187. (Full text)

Na+-K+ pump activities of high- and low-potassium sheep red cells with internal magnesium and calcium altered by A23187. 1. Sheep erythrocytes were treated with the divalent metal ionophore A23187 to alter the cellular magnesium (Mgi) and calcium (Cai) composition. Ouabain-sensitive Na+-K+ pump fluxes were measured using rubidium as a potassium congener in media where Cl- was replaced by NO3-. 2. A23187, per se, had no effect on ouabain-sensitive rubidium influx. However, lowering (...) the concentration of cellular magnesium [( Mg]i) and increasing that of calcium [( Ca]i) decreased Na+-K+ pump flux. 3. Ouabain-sensitive rubidium influx was found to be a saturating function of [Mg]i in high-potassium (HK) red cells with a Hill coefficient of about 1.8 and an apparent half-activation constant (K0.5) of 0.46 mmol/(l original cells). In low-potassium (LK) cells, in the absence and presence of the Na+-K+ pump stimulatory L-antibody, ouabain-sensitive rubidium influx was also saturated with Mgi

1988 The Journal of physiology PubMed abstract

4330. The effects of rubidium ions on components of the potassium conductance in the frog node of Ranvier. (Full text)

The effects of rubidium ions on components of the potassium conductance in the frog node of Ranvier. The effects of replacement of external and internal K+ ions by Rb+ ions on the two fast components (gf1 and gf2) and slow component (gs) of the K+ conductance (gK) in frog nodes of Ranvier were investigated under voltage- and current-clamp conditions. Fast and slow components of gK were separated by double exponential fits to tail currents following long depolarizing pre-pulses, or by the use (...) component of the tail current. Regenerative responses, which occur in high [K+] (+300 nM-tetrodotoxin) solutions in current clamp did not repolarize in Rb+. Voltage-clamp experiments showed that inactivation of inward currents is slowed when Rb+ is the charge carrier. Replacement of internal K+, by application of Rb+ to the cut ends of the fibre, shifted the reversal potential to more positive potentials but had no effect on the conductance or kinetics. External Rb+ has a large number of effects

1986 The Journal of physiology PubMed abstract

4331. Modulation of potassium conductances by an endogenous neuropeptide in neurones of Aplysia californica. (Full text)

Modulation of potassium conductances by an endogenous neuropeptide in neurones of Aplysia californica. 1. Macroscopic and single-channel currents were recorded from voltage-clamped neurones in the abdominal and pleural ganglia of Aplysia californica in order to investigate conductance changes elicited by application of the endogenous peptide FMRFamide (Phe-Met-Arg-Phe-NH2) and related neuropeptides to the cell surface. 2. The Ca-dependent K current, IK(Ca), when elicited at a constant voltage (...) by intracellular injection of Ca2+, was insensitive to FMRFamide or its derivative YGG-FMRFamide (Tyr-Gly-Gly-Phe-Met-Arg-Phe-NH2). 3. Under steady voltage clamp, certain cells responded to a brief puff of FMRFamide or YGG-FMRFamide with a transient outward current lasting about 1 min. Unclamped cells responded with a corresponding hyperpolarization. These responses reversed at about -75 mV. Ion substitution indicated that the current is carried by K+. 4. FMRFamide and YGG-FMRFamide were equally effective

1987 The Journal of physiology PubMed abstract

4332. Effects of external calcium on potassium contractures in tonic muscle fibers of the frog (Rana pipiens). (Full text)

Effects of external calcium on potassium contractures in tonic muscle fibers of the frog (Rana pipiens). K+ contractures of tonic bundles from cruralis muscle of the frog were studied with different K+ concentrations (10-120 mM). K+ contractures had an initial transient phase followed by a sustained tension. The amplitude of the sustained tension diminished with high K+ concentration (80-120 mM). However, in all cases, tension was maintained for several minutes. External Ca2+ reduction (...) + substitution for Ca2+ before or during K+ contractures. These results indicate that external Ca2+ had to be continuously present to maintain the tension during K+ contractures and that Ni2+ was not able to restore the normal temporal course of K+ contracture. The sustained phase was diminished by blocking agents of Ca2+ channels, such as nifedipine (1 microM) and diltiazem (1-10 microM). The present results can be explained by a direct control of the Ca2+ currents on K+ contracture or by specific

1986 The Journal of physiology PubMed abstract

4333. Potassium uptake in the mouse submandibular gland is dependent on chloride and sodium and abolished by piretanide. (Full text)

+ uptake was, however, unaffected when Br- replaced Cl- in the superfusate. Similar effects were observed in the unstimulated glandular tissues. The introduction of Cl-(-)free media containing either NO3- or SO4(2-) resulted in a loss of K+ from the tissue which was followed, upon reintroduction of Cl-, by a pronounced uptake of K+. When Br- was substituted for Cl- there was very little change in [K+] upon removal or reintroduction of Cl-. The uptake of K+ induced by reintroduction of Cl- after (...) Potassium uptake in the mouse submandibular gland is dependent on chloride and sodium and abolished by piretanide. Nervous or hormonal stimulation of salivary secretion in vivo is associated with a pronounced efflux of K+ from the secretory, acinar cells into the blood. This K+ efflux is followed in the post-stimulus period by a reuptake of K+ into the glandular tissue. In the present study we monitor the changes in [K+] of physiological solutions perfusing a flow chamber containing isolated

1986 The Journal of physiology PubMed abstract

4334. Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle. (Full text)

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle. 1. Unitary currents were measured through delayed rectifier potassium channels of frog skeletal muscle, under conditions where either potassium or rubidium ions carried current. 2. Unitary currents were reduced in amplitude when Rb+ was the charge carrier, indicating that Rb+ permeated the channel less readily than did K+. On the other hand permeability ratios (PRb/PK) measured from the change (...) in reversal potential upon ionic substitution were 0.92 for the external and 0.67 for the internal mouth of the channel. 3. Ensemble-averaged currents activated under depolarization along a similarly S-shaped time course whether K+ or Rb+ carried current, though slightly more slowly in Rb+. However, under repolarization to a negative level, tail currents were prolonged about tenfold in Rb+. 4. The duration of channel opening was substantially prolonged in Rb+. The distribution of open times was fitted

1989 The Journal of physiology PubMed abstract

4335. Potassium (86Rb+) efflux from the rat submandibular gland under sodium-free conditions in vitro. (Full text)

Potassium (86Rb+) efflux from the rat submandibular gland under sodium-free conditions in vitro. 1. Fragments of rat submandibular gland were pre-loaded with 86Rb+, an isotopic marker of potassium transport, and rate constants for 86Rb+ efflux were determined during superfusion with a physiological salt solution. 2. In sodium-containing solutions acetylcholine evoked a rapid and immediate increase in efflux rate. After reaching a peak value, the efflux rate initially declined rapidly (...) , but a second, slowly declining phase to the response was also evident. The response could be resolved into Ca2(+)-independent and Ca2(+)-dependent phases. 3. The basal efflux rate was elevated during superfusion with solutions in which sodium had been replaced with either lithium or N-methyl-D-glucammonium (NMDG+). Although lithium had a greater effect, which was absent under calcium-free conditions, addition of calcium to initially calcium-free, lithium-containing solutions did not affect the rate

1989 The Journal of physiology PubMed abstract

4336. Thapsigargin inhibits a potassium conductance and stimulates calcium influx in the intact rat lens (Full text)

Thapsigargin inhibits a potassium conductance and stimulates calcium influx in the intact rat lens 1. An increase in lens cell calcium has long been associated with cortical cataract. Recently, it has been shown that thapsigargin induces a rise in lens cell calcium by release from endoplasmic reticulum stores. The effects of this rise on the optical and membrane characteristics of the lens were studied in the isolated rat lens. 2. The electrical characteristics of the isolated, perifused rat (...) lens were measured using a two-internal microelectrode technique that permits measurement of plasma membrane conductance (Gm), membrane potential (Vm) and junctional conductance in the intact lens. 3. Thapsigargin (1 microM) induced a rapid overall depolarization of Vm that was accompanied by first a decrease and then an increase in Gm. 4. Replacing external Na+ with tetraethylammonium (TEA) abolished the decrease in Gm. However, a transient increase phase was still observed. 5. The changes

1999 The Journal of physiology PubMed abstract

4337. The dependence of Ag+ block of a potassium channel, murine Kir2.1, on a cysteine residue in the selectivity filter (Full text)

The dependence of Ag+ block of a potassium channel, murine Kir2.1, on a cysteine residue in the selectivity filter Externally applied Ag+ (100-200 nM) irreversibly blocked the strong inwardly rectifying K+ channel, Kir2.1. Mutation to serine of a cysteine residue at position 149 in the pore-forming H5 region of Kir2.1 abolished Ag+ blockage. To determine how many of the binding sites must be occupied by Ag+ before the channel is blocked, we measured the rate of channel block and found that our (...) results were best fitted assuming that only one Ag+ ion need bind to eliminate channel current. We tested our hypothesis further by constructing covalently linked dimers and tetramers of Kir2.1 in which cysteine had been replaced by serine in one (dimer) or three (tetramer) of the linked subunits. When expressed, these constructs yielded functional channels with either two (dimer) or one (tetramer) cysteines per channel at position 149. Blockage in the tetramer was complete after sufficient exposure

1998 The Journal of physiology PubMed abstract

4338. The selectivity filter of a potassium channel, murine Kir2.1, investigated using scanning cysteine mutagenesis (Full text)

The selectivity filter of a potassium channel, murine Kir2.1, investigated using scanning cysteine mutagenesis We have produced a structural model of the pore-forming H5 (or P) region of the strong inward rectifier K+ channel, Kir2.1, based initially on an existing molecular model of the pore region of the voltage-gated K+ channel, Kv1.3. Cysteine-scanning mutagenesis and subsequent blockage by Ag+ was used to test our model by determining the residues in H5 whose side chains line the ion (...) conduction pathway. Mutations made in eight positions within the highly conserved H5 region resulted in apparently non-functional channels. Constructing covalently linked dimers, which carry a cysteine substitution in only one of the linked subunits, rescued six of these mutants; a covalently linked tetramer, carrying a cysteine substitution on only one of the linked subunits, rescued a further mutant. Our results using the dimers and tetramers suggest that residues Thr141, Thr142, Ile143, Tyr145, Phe147

1998 The Journal of physiology PubMed abstract

4339. Mutations of the S4-S5 linker alter activation properties of HERG potassium channels expressed in Xenopus oocytes (Full text)

Mutations of the S4-S5 linker alter activation properties of HERG potassium channels expressed in Xenopus oocytes 1. The structural basis for the activation gate of voltage-dependent K+ channels is not known, but indirect evidence has implicated the S4-S5 linker, the cytoplasmic region between the fourth and fifth transmembrane domains of the channel subunit. We have studied the effects of mutations in the S4-S5 linker of HERG (human ether-รก-go-go-related gene), a human delayed rectifier K (...) . In response to large hyperpolarizations, D540K HERG channels can reopen into a state that is distinct from the normal depolarization-induced open state. It is proposed that substitution of a negatively charged Asp with the positively charged Lys disrupts a subunit interaction that normally stabilizes the channel in a closed state at negative transmembrane potentials. 5. The results indicate that the S4-S5 linker is a crucial component of the activation gate of HERG channels.

1999 The Journal of physiology PubMed abstract

4340. Role of TASK2 Potassium Channels Regarding Volume Regulation in Primary Cultures of Mouse Proximal Tubules (Full text)

Role of TASK2 Potassium Channels Regarding Volume Regulation in Primary Cultures of Mouse Proximal Tubules Several papers reported the role of TASK2 channels in cell volume regulation and regulatory volume decrease (RVD). To check the possibility that the TASK2 channel modulates the RVD process in kidney, we performed primary cultures of proximal convoluted tubules (PCT) and distal convoluted tubules (DCT) from wild-type and TASK2 knockout (KO) mice. In KO mice, the TASK2 coding sequence (...) was in part replaced by the lac-Z gene. This allows for the precise localization of TASK2 in kidney sections using beta-galactosidase staining. TASK2 was only localized in PCT cells. K+ currents were analyzed by the whole-cell clamp technique with 125 mM K-gluconate in the pipette and 140 mM Na-gluconate in the bath. In PCT cells from wild-type mice, hypotonicity induced swelling-activated K+ currents insensitive to 1 mM tetraethylammonium, 10 nM charybdotoxin, and 10 microM 293B, but blocked by 500

2003 The Journal of general physiology PubMed abstract

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