Electrogenic Na+ Transport in a Crustacean Coxal Receptor

1979 ◽  
Vol 78 (1) ◽  
pp. 29-45
Author(s):  
MAURIZIO MIROLLI
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Input Resistance ◽  
Scylla Serrata ◽  
Partial Action ◽  
State Response ◽  
Electrogenic Na Pump ◽  
K Concentration ◽  
Low K ◽  
In Cells

1. The response of the coxal receptors of the crab Scylla serrata to step stretches consisted of a partial action potential, Vα, followed by a steady-state depolarization, V8. The input resistance of the fibre was reduced during V8. 2. In the absence of stimulation, the dendrites of the receptors depolarized when external Na+ was substituted with choline or Li+, and when the external K+ concentration was increased or decreased. The dendrites also depolarized when ouabain was added to the saline. 3. The amplitude of both Vα and V8 was dependent on external Na+. In cells which were depolarized by ouabain, the amplitude of V8 increased when the K+ concentration of the saline was reduced. 4. V8 was followed by a small, but long-lasting, after-potential which was depolarizing when the membrane potential was between −70 and −60 mV. In cells depolarized by ouabain or by low K+ saline, the after-potential became hyperpolarizing. 5. When trains of brief stretches (each 5 ms in duration) were used as stimuli, the cells responded with trains of Vα responses. During this tetanic stimulation the cells hyperpolarized; cessation of the stimulus train was followed by a long-lasting hyperpolarization (PTH). 6. PTH was abolished in Li+ saline, in low K+ saline, and in the presence of ouabain. In control or in low K+ saline, PTH was not accompanied by a decrease in the input resistance of the fibres. 7. It is concluded that an electrogenic Na+ pump (or equivalent process) contributes a substantial fraction of the membrane potential of the unstimulated coxal receptors. Pump activity could be increased by Na+-loading the distal part of the cells with trains of Vα responses. By contrast, during the steady-state response to stretch, the pump was not activated.

Effects of ouabain on background and voltage-dependent currents in canine colonic myocytes

1990 ◽  
Vol 259 (3) ◽  
pp. C402-C408 ◽  
Author(s):  
E. P. Burke ◽  
K. M. Sanders
Keyword(s):  
Membrane Potential ◽  
Potential Gradient ◽  
Circular Muscle ◽  
Input Resistance ◽  
Pump Current ◽  
Muscle Layer ◽  
Membrane Properties ◽  
Resting Potential ◽  
Voltage Dependent ◽  
In Cells

Previous studies have suggested that the membrane potential gradient across the circular muscle layer of the canine proximal colon is due to a gradient in the contribution of the Na(+)-K(+)-ATPase. Cells at the submucosal border generate approximately 35 mV of pump potential, whereas at the myenteric border the pump contributes very little to resting potential. Results from experiments in intact muscles in which the pump is blocked are somewhat difficult to interpret because of possible effects of pump inhibitors on membrane conductances. Therefore, we studied isolated colonic myocytes to test the effects of ouabain on passive membrane properties and voltage-dependent currents. Ouabain (10(-5) M) depolarized cells and decreased input resistance from 0.487 +/- 0.060 to 0.292 +/- 0.040 G omega. The decrease in resistance was attributed to an increase in K+ conductance. Studies were also performed to measure the ouabain-dependent current. At 37 degrees C, in cells dialyzed with 19 mM intracellular Na+ concentration [( Na+]i), ouabain caused an inward current averaging 71.06 +/- 7.49 pA, which was attributed to blockade of pump current. At 24 degrees C or in cells dialyzed with low [Na+]i (11 mM), ouabain caused little change in holding current. With the input resistance of colonic cells, pump current appears capable of generating at least 35 mV. Thus an electrogenic Na+ pump could contribute significantly to membrane potential.

Relation of membrane potential to basolateral TEA transport in isolated snake proximal renal tubules

1995 ◽  
Vol 268 (6) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Y. K. Kim ◽  
W. H. Dantzler
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Potent Inhibitor ◽  
Basolateral Membrane ◽  
Potential Difference ◽  
Renal Tubules ◽  
K Concentration ◽  
Electrochemical Equilibrium ◽  
Membrane Potential Difference ◽  
Basolateral Membrane Potential

We measured the effects of changes in bath K+ concentration ([K+]) on basolateral membrane potential difference (PD) and [3H]tetraethylammonium (TEA) transport in isolated snake (Thamnophis) proximal renal tubules (25 degrees C; pH 7.4). Increasing bath [K+] from 3 to 65 mM decreased PD from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA by approximately 25%, indicating that PD influences TEA entry into the cells. Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by unlabeled TEA, indicating that uptake is carrier mediated. Kt (approximately 18 microM) for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM K+, suggesting that the decrease in PD or the increase in [K+] alters the affinity of the transporter for TEA. The steady-state cell-to-bath ratio for [3H]TEA with 3 mM K+ (-60 mV PD) was approximately 16, significantly above the ratio of 10 predicted for passive distribution at electrochemical equilibrium. With 65 mM K+ (-20 mV PD) this ratio decreased to approximately 6, again significantly above the predicted ratio of 2. These data suggest that the PD can account for much, but not all, of the steady-state uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was identical with either 3 or 65 mM K+ in the bath but was almost completely inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA uptake. These data indicate that virtually all TEA transport across the basolateral membrane is carrier mediated and that transport out of the cells is unaffected by PD.

scholarly journals Cat Heart Muscle in Vitro

1965 ◽  
Vol 48 (5) ◽  
pp. 933-948 ◽  
Author(s):  
Jon Goerke ◽  
Ernest Page
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Papillary Muscle ◽  
Heart Muscle ◽  
Volume Ratio ◽  
K Concentration ◽  
Linear Manner ◽  
Cat Heart ◽  
External K

The exchange of cell K with K42, JK, has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. JK increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, PK, calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. JK is not affected by replacement of O2 by N2, or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10-5 M and 10-8 M ouabain.

Acute resetting of carotid sinus baroreceptors. II. Possible involvement of electrogenic Na+ pump

1984 ◽  
Vol 247 (5) ◽  
pp. H833-H839 ◽  
Author(s):  
C. M. Heesch ◽  
F. M. Abboud ◽  
M. D. Thames
Keyword(s):  
Single Unit ◽  
Carotid Sinus ◽  
Threshold Pressure ◽  
Carotid Sinus Nerve ◽  
Na Pump ◽  
Electrogenic Na Pump ◽  
Before And After ◽  
K Concentration ◽  
Low K ◽  
Sinus Pressure

In the accompanying manuscript [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H824-H832, 1984] we demonstrated that a mechanical mechanism alone cannot account for acute resetting of baroreceptors. To determine if changes in the activity of a baroreceptor electrogenic Na+ pump contributed to resetting, single-unit baroreceptor discharge was recorded from the carotid sinus nerve while resetting protocols were performed before and after exposing the vascularly isolated carotid sinus to treatments known to block the Na+ pump [ouabain and low extracellular K+ concentration ([K+]o)]. Ouabain (0.1-0.5 microgram/ml) blocked the increase in baroreceptor threshold pressure that occurred when intrasinus pressure was increased by 30 mmHg for 15 min [delta threshold = 16 +/- 3 (SE) mmHg before and 1.2 +/- 2.3 mmHg after ouabain]. In 12 experiments carotid sinus pressure was increased from 70 to 160 mmHg for 5 min and then returned to 70 mmHg for 10 min in the presence of both normal [K+]o (5.8 mM) and low [K+]o. Exposure to the low K+ solution resulted in a significantly smaller increase in threshold pressure when intrasinus pressure was increased from 70 to 160 mmHg (9 +/- 2.7 vs. 18 +/- 2.1 mmHg). When K+ was replaced, threshold pressure again increased by 18 +/- 2.3 mmHg, the increase in threshold was reversed. Thus, since ouabain blocked and low [K+]o attenuated acute resetting of the baroreceptors, we propose that changes in the activity of an electrogenic Na+ pump contribute to acute resetting.

Electrogenic sodium pumping in rabbit small intestinal smooth muscle

1975 ◽  
Vol 229 (5) ◽  
pp. 1277-1286 ◽  
Author(s):  
TY El-Sharkawy ◽  
EE Daniel
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Membrane Potential ◽  
Intestinal Smooth Muscle ◽  
Ionic Mechanism ◽  
Control Potential ◽  
Normal Tissues ◽  
Na Pump ◽  
Electrogenic Na Pump ◽  
Small Intestinal

Oscillations in the activity of an electrogenic Na pump has been suggested as the ionic mechanism underlying the intestinal control potential (slow wave). We investigated the electrogenicity of this pump in rabbit jejunal smooth muscle. Potassium admission to Na-rich tissues caused a large increase in membrane potential which after 10--20 min decreased toward values comparable with those of normal tissues. This hyperpolarization far exceeded EK and could be prevented by cooling or by ouabain. No hyperpolarization occurred upon K admission to Li-rich tissues in the absence of Na. Thus, the pump in this tissue can operate electrogenically. Goldman's equation was modified so as to account for the pump's contribution to the membrane potential. Using this equation, the calculated contribution of the pump, under normal "steady-state" conditions, is unlikely to exceed a few millivolts. It is concluded that although the pump in this tissue can be electrogenic, its contribution may be smaller than that required if the intestinal control potential resulted from rhythmic turning off and on of the electrogenic Na pump.

Rat hippocampal astrocytes exhibit electrogenic sodium-bicarbonate co-transport

1994 ◽  
Vol 72 (6) ◽  
pp. 2580-2589 ◽  
Author(s):  
E. R. O'Connor ◽  
H. Sontheimer ◽  
B. R. Ransom
Keyword(s):  
Membrane Potential ◽  
Reversal Potential ◽  
Input Resistance ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Induced Response ◽  
Potential Range ◽  
Free Solution ◽  
Hippocampal Astrocytes ◽  
In Cells

1. We probed for the expression of electrogenic Na+/HCO3- co-transport in cultured mammalian astrocytes by recording voltage and current changes induced by bath application of HCO3-, with the use of patch-clamp electrophysiology. Application of 25 mM HCO3-, at a constant pHo, to astrocytes bathed in a nominally HCO3(-)-free solution, produced an abrupt and reversible change in membrane potential ranging from +3 to -30 mV [-11.8 +/- 9.34 (SD) mV]; 55% of cells showed relatively large hyperpolarizing responses (-18.8 +/- 6.23 mV), whereas 45% showed only small shifts in membrane potential (range of -5 to +3 mV; -1.9 +/- 1.96 mV). 2. The size of the HCO3(-)-induced hyperpolarization was strongly related to the cell's initial resting membrane potential in HCO3(-)-free solution; the larger responses were seen in cells with relatively low resting membrane potentials (-48.5 +/- 9.4 mV), and the smaller responses were seen in cells with more negative potentials (-68.1 +/- 6.5 mV). The membrane potentials of hippocampal astrocytes were highly variable in HCO3(-)-free solution (range -38 to -80 mV; -60.9 +/- 12.53); this variability was greatly reduced in HCO3(-)-containing solution (range -59 to -82 mV; -68.5 +/- 4.8). 3. The magnitude of the HCO3(-)-induced response was less strongly correlated with cell input resistance, which was higher in the larger responder cells than in the small responders. However, the differences in input resistance were insufficient to account for the different HCO3(-)-induced responses observed. 4. In the presence of extracellular Ba2+, which by blocking K+ conductance depolarized cells by 30-50 mV, cells that initially showed a small response, showed a large and completely reversible hyperpolarization (-18.4 +/- 6.13 mV) to application of 25 mM HCO3-. In Na(+)-free solution, the HCO3(-)-induced hyperpolarization was reduced by 66%, and the response was not sustained, as in Na(+)-containing solution. Removal of extracellular Cl- had no effect on the HCO3- response The stilbene derivative 4,4'-diisothiocyano-2,2'-stilbene disulfonate (DIDS), a blocker of anion transport, eliminated the HCO3(-)-induced hyperpolarization. Blockers of Na+/K+ ATPase and Na(+)-H+ exchange were without effect. These observations indicated the presence of an electrogenic Na+/HCO3- co-transporter in hippocampal astrocytes. 6. Voltage-clamp recording demonstrated that the HCO3(-)-induced hyperpolarization was caused by outward currents averaging 335 +/- 104 pA. The reversal potential of the HCO3(-)-induced current ranged between -80 and -99 mV with an average = -86.1 +/- 6.2 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Unidirectional flux ratio for potassium ions in depolarized frog skeletal muscle

1981 ◽  
Vol 241 (1) ◽  
pp. C68-C75 ◽  
Author(s):  
B. C. Spalding ◽  
O. Senyk ◽  
J. G. Swift ◽  
P. Horowicz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Flux Ratio ◽  
External Solution ◽  
Resting Potential ◽  
Frog Skeletal Muscle ◽  
High K ◽  
Sigmoidal Curve ◽  
K Concentration ◽  
Low K

Small bundles of frog skeletal muscle fibers were loaded with 305 mM K+ and 120 mM Cl-, and 42K+ tracer efflux and influx were measured as a function of external K+ concentration ([K+]o) at a resting potential of -2 mV. As [K+]o was lowered from 305 mM, efflux decreased along a markedly sigmoidal curve, reaching a constant nonzero value at low [K+]o. Influx varied linearly with [K+]o at low [K+]o and more steeply at higher [K+]o. The ratio of influx to efflux was described by the equation: influx/efflux = exp[-n(V - VK)F/RT] with n = 2 at high [K+]o, but the ratio approached this equation with n = 1 at low [K+]o. Efflux did not depend on [K+]o when the membrane potential was raised to +36 mV, whereas at low [K+]o decreasing the membrane potential to -19 mV further activated the efflux. The results are discussed in terms of an inwardly rectifying potassium channel with two or more activating sites within the membrane that bind K+ and are accessible from the external solution.

An examination of frog myelinated axons using intracellular microelectrode recording: the role of voltage-dependent and leak conductances on the steady-state electrical properties

1993 ◽  
Vol 70 (6) ◽  
pp. 2301-2312 ◽  
Author(s):  
M. O. Poulter ◽  
T. Hashiguchi ◽  
A. L. Padjen
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Input Resistance ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
External Application ◽  
Barium Ions ◽  
Anomalous Rectification ◽  
Outward Rectification ◽  
A Current

1. Intracellular microelectrode current-clamp technique was used to study the steady-state membrane properties of single intact large primary afferent axons (conduction velocity > 10 m/s) attached to isolated hemisected frog spinal cord. 2. Hyperpolarizing electrotonic potentials (ETPs) had a slow complex multiphasic charging. This complex charging could be approximated by two time constants: one in the range of 70–210 ms, the other of < 20 ms. 3. Two regions of outward and inward rectification hyperpolarized to the resting membrane potential were observed, in addition to the previously characterized outward rectification active at potentials depolarized to resting membrane potential. The peak and steady-state input resistance of these axons in tetrodotoxin Ringer solution was on average 65.6 +/- 21.1 and 31.1 +/- 10.8 M omega, mean +/- SE, respectively. 4. Application of external tetraethylammonium (10–20 mM) significantly depolarized the axon and decreased the outward rectification just hyperpolarized to the resting membrane potential. This outward rectification could also be blocked by external barium ions (2–10 mM). 5. Activation of an inward or anomalous rectification in these axons was observed 300–600 ms after the start of a current pulse. In addition, a depolarizing afterpotential (DAP) (1–3 mV in amplitude, 500 ms-10 s in duration) was evident after a current pulse in which inward rectification had been activated. This DAP most likely reflected the slow inactivation of the inwardly rectifying conductance. 6. Inward rectification was blocked by external application of cesium ions (1–3 mM) but it was insensitive to external application of barium ions (2–10 mM). The blockade of the voltage attenuation was accompanied by a disappearance of the DAP and an increase in the charging time constant of the axon. This blockade resulted in a single linear voltage-current (V-I) relationship. Axons now had, on average, an input resistance of 114 +/- 19.1 M omega. 7. Reducing the concentration of external potassium ions increased both the peak and steady-state slope resistance. Reducing the external sodium concentration altered the ETPs and the V-I relationship little but it consistently reduced the magnitude and length of the DAP. These results are compatible with the hypothesis that anomalous rectification is a mixed ionic conductance dependent on potassium and sodium ions in the external media. 8. Overall, the V-I relationship of these intact axons had both linear and nonlinear regions reflecting the activity of numerous slowly activating and inactivating conductances. (ABSTRACT TRUNCATED AT 400 WORDS)

Changes in Membrane Properties of the Drosophila Dorsal Longitudinal Flight Muscle Induced by Sodium Pump Inhibitors

1981 ◽  
Vol 90 (1) ◽  
pp. 175-183 ◽  
Author(s):  
BARBARA K. HENON ◽  
KAZUO IKEDA
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Sodium Pump ◽  
Flight Muscle ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Slow Phase ◽  
Muscle Fibres ◽  
Fast Phase ◽  
In Cells

1. Drosophila dorsal longitudinal flight muscle fibres made anoxic by passing nitrogen through the tracheal system or treated with 10−5M ouabain or strophanthidin show a reversible fall in resting membrane potential of 16·5 mV (S.E. 0·96), 1·37 mV (S.E. 0·87), and 1·70 mV (S.E. 2·8), respectively. The reversible depolarization obtained with these sodium pump blockers occurred within 10–15 min. 2. The depolarization of the muscle fibres was accompanied by a decrease in input resistance of 21·2% (S.E. 3·8) in anoxia, 21·4% in ouabain, and 25·6% (S.E. 6·7) in strophanthidin. The resistance decrease in strophanthidin and ouabain was transient and returned to above the resting level while the muscle fibres were still exposed to these agents. 3. Recovery of membrane potential in cells exposed to anoxia is biphasic. An initial ‘fast’ phase of recovery occurs within 15 s upon return to air followed by a late ‘slow’ phase lasting several minutes. Recovery of input resistance in cells exposed to N2 coincided with the ‘fast’ phase of the recovery of resting membrane potential. 4. Recovery of membrane potential following exposure to strophanthidin is a long, slow process which occurs at conductance values at the resting level or below. 5. The tendency towards spontaneous action potentials was increased by anoxia and the action potentials occurring in anoxia were elongated into plateau potentials of about 18s duration. 6. These results are consistent with the hypothesis that anoxia and cardioactive steroids inhibit a metabolic process, possibly an electrogenic ion pump, that is essential for maintenance of the resting membrane potential in Drosophila flight muscle. Exposure to these agents also results in changes in input resistance. Both of these effects could contribute to the depolarization and affect the excitable properties of the muscle fibre membrane.

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