Voltage-dependent effects of isoproterenol on cytosolic Ca concentration in rat heart

The effect of the beta-adrenoceptor agonist, isoproterenol, on cytosolic calcium concentration ([Ca2+]i) was studied with the Ca2+-sensitive fluorescent indicator quin 2 in enzymatically dissociated rat ventricular myocytes. Under conditions in which cells have normal polarized resting membrane potential, isoproterenol (1 microM) produced a decrease in [Ca2+]i. In contrast, in the depolarized cells (by raising extracellular K+ concentration to 50 mM), isoproterenol (1 microM) caused an increase in [Ca2+]i. This isoproterenol-induced increase in [Ca2+]i in depolarized cells could be reversed by prior exposure of the cells to the Ca2+ channel blocker, verapamil (5 microM). The results indicate that isoproterenol can either decrease or increase [Ca2+]i depending on membrane potential. The actual effect of isoproterenol on [Ca2+]i at any given membrane potential probably reflects the relative contributions of isoproterenol-induced stimulation of Ca2+ buffering or effluxing activities (which favor a decrease in [Ca2+]i) and enhancement of Ca2+ influx through voltage-sensitive Ca2+ channels (which favors an increase in [Ca2+]i).

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Inhibition of voltage-dependent Ca2+influx by extracellular ATP in salivary cells of the leech Haementeria ghilianii

Journal of Experimental Biology ◽

10.1242/jeb.199.6.1335 ◽

1996 ◽

Vol 199 (6) ◽

pp. 1335-1341

Author(s):

W Wuttke ◽

T Munsch ◽

J Deitmer

Keyword(s):

Membrane Potential ◽

Voltage Clamp ◽

Extracellular Atp ◽

Threshold Concentration ◽

Resting Membrane Potential ◽

Voltage Gated ◽

Voltage Dependent ◽

K Concentration ◽

Gamma S ◽

Ca2 Channels

The effects of extracellular ATP on intracellular free Ca2+ concentration ([Ca2+]i) and depolarization-induced elevations of [Ca2+]i were investigated in salivary cells of the leech Haementeria ghilianii using the fluorescent Ca2+ indicator Fura-2. Simultaneously, the membrane potential was monitored or controlled by voltage-clamp. The cell membrane was depolarized either by transient elevations of the extracellular K+ concentration ([K+]o) to 90 mmol l-1 or by depolarizing steps under voltage-clamp. The resulting transient elevations of [Ca2+]i (Ca2+ transients) could be repeatedly elicited with little variability in amplitude. Ca2+ transients were completely inhibited by 2 mmol l-1 Ni2+ or in Ca2+-free saline. The transients are, therefore, dependent on Ca2+ influx from the external medium through voltage-gated Ca2+ channels. The Ca2+ influx was rapidly and reversibly inhibited by extracellular application of ATP. The effect was dose-dependent with a threshold concentration below 10(-7) mol l-1. A 50 % reduction in the amplitude of Ca2+ transients was obtained by application of 12 µmol l-1 ATP or ATP-gamma-S (apparent IC50, 1.6 µmol l-1 ATP) and Ca2+ transients were almost completely inhibited by 30100 µmol l-1 ATP. Resting [Ca2+]i, the resting membrane potential and membrane potential changes induced by 90 mmol l-1 [K+]o were not affected by ATP. Adenosine (10 µmol l-1) did not affect resting [Ca2+]i, the resting membrane potential or membrane potential changes induced by 90 mmol l-1 [K+]o and had little effect on Ca2+ transients. Suramin, an antagonist of vertebrate P2 receptors, was without effect on the inhibitory actions of ATP. We conclude that activation of a suramin-insensitive purinoceptor by ATP inhibits Ca2+ influx through voltage-gated Ca2+ channels in the salivary cells of Haementeria ghilianii.

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Calcium channels and control of cytosolic calcium in rat and bovine zona glomerulosa cells

AJP Cell Physiology ◽

10.1152/ajpcell.1992.262.3.c598 ◽

1992 ◽

Vol 262 (3) ◽

pp. C598-C606 ◽

Cited By ~ 25

Author(s):

S. J. Quinn ◽

U. Brauneis ◽

D. L. Tillotson ◽

M. C. Cornwall ◽

G. H. Williams

Keyword(s):

Membrane Potential ◽

Voltage Clamp ◽

Cell Voltage ◽

Cytosolic Calcium ◽

Zona Glomerulosa ◽

Voltage Dependent ◽

Low Threshold ◽

K Concentration ◽

Ca2 Channels ◽

External K

Rat and bovine adrenal zona glomerulosa (ZG) cells possess a low-threshold, voltage-dependent Ca2+ current that was characterized using whole cell voltage clamp techniques. Activation of this current is observed at membrane potentials above -80 mV with maximal peak Ca2+ current elicited near -30 mV. Inactivation of the Ca2+ current was half-maximal between -74 and -58 mV, depending on the external Ca2+ concentration and was nearly complete at -40 mV. The voltage dependency of the current indicates that a calcium current could be sustained at membrane potentials between -80 and -40 mV and thereby elevates cytosolic calcium (Cai) levels. Under basal conditions, Cai is stable in single rat ZG cells, whereas more than half of the bovine ZG cells produce repeated Cai transients. These Cai transients, which are blocked by removal of external Ca2+ or addition of Ni2+, are likely due to repetitive electrical activity in bovine ZG cells. Cai responses can be elicited by small increases in external K+ concentration (5-10 mM) in both rat and bovine ZG cells, indicating the opening of low-threshold Ca2+ channels. However, these Cai changes remain robust at high external K+ concentrations (20-40 mM). In experiments combining Cai measurements and whole cell voltage clamp, a steep dependence of Cai on membrane potential was revealed beginning at depolarizing voltages near a holding membrane potential of -80 mV. A maximal increase in Cai occurred near -30 mV (equivalent to an external K+ concentration of 40 mM), a membrane voltage at which sustained current through low-threshold Ca2+ channels should be negligible. These data raise the possibility of additional voltage-dependent pathways for Ca2+ influx.

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Anesthetic Effects on Resting Membrane Potential Are Voltage-dependent and Agent-specific

Anesthesiology ◽

10.1097/00000542-199101000-00014 ◽

1991 ◽

Vol 74 (1) ◽

pp. 83-88 ◽

Cited By ~ 35

Author(s):

M. Bruce Maclver ◽

Joan J. Kendig

Keyword(s):

Membrane Potential ◽

Resting Membrane Potential ◽

Voltage Dependent

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Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00499.2005 ◽

2007 ◽

Vol 292 (1) ◽

pp. R388-R395 ◽

Cited By ~ 10

Author(s):

Cristina E. Molina ◽

Hans Gesser ◽

Anna Llach ◽

Lluis Tort ◽

Leif Hove-Madsen

Keyword(s):

Membrane Potential ◽

Action Potential ◽

Ventricular Myocytes ◽

Reversal Potential ◽

Membrane Potentials ◽

Resting Membrane Potential ◽

Atrial Myocytes ◽

Atrial Tissue ◽

Isolated Cardiac Myocytes ◽

Inwardly Rectifying

Application of the current-clamp technique in rainbow trout atrial myocytes has yielded resting membrane potentials that are incompatible with normal atrial function. To investigate this paradox, we recorded the whole membrane current ( Im) and compared membrane potentials recorded in isolated cardiac myocytes and multicellular preparations. Atrial tissue and ventricular myocytes had stable resting potentials of −87 ± 2 mV and −83.9 ± 0.4 mV, respectively. In contrast, 50 out of 59 atrial myocytes had unstable depolarized membrane potentials that were sensitive to the holding current. We hypothesized that this is at least partly due to a small slope conductance of Im around the resting membrane potential in atrial myocytes. In accordance with this hypothesis, the slope conductance of Im was about sevenfold smaller in atrial than in ventricular myocytes. Interestingly, ACh increased Im at −120 mV from 4.3 pA/pF to 27 pA/pF with an EC50 of 45 nM in atrial myocytes. Moreover, 3 nM ACh increased the slope conductance of Im fourfold, shifted its reversal potential from −78 ± 3 to −84 ± 3 mV, and stabilized the resting membrane potential at −92 ± 4 mV. ACh also shortened the action potential in both atrial myocytes and tissue, and this effect was antagonized by atropine. When applied alone, atropine prolonged the action potential in atrial tissue but had no effect on membrane potential, action potential, or Im in isolated atrial myocytes. This suggests that ACh-mediated activation of an inwardly rectifying K+ current can modulate the membrane potential in the trout atrial myocytes and stabilize the resting membrane potential.

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The hyperpolarization-activated current shifts the dynamic range of a voltage-dependent electrical synapse

10.1101/2021.12.16.472972 ◽

2021 ◽

Author(s):

Wolfgang Stein ◽

Margaret DeMaegd ◽

Lena Yolanda Braun ◽

Andrés G Vidal-Gadea ◽

Allison L Harris ◽

...

Keyword(s):

Membrane Potential ◽

Motor Neuron ◽

Axon Terminal ◽

Voltage Dependence ◽

Dynamic Range ◽

Complex Dynamics ◽

Ionic Current ◽

Electrical Synapse ◽

Resting Membrane Potential ◽

Voltage Dependent

Like their chemical counterparts, electrical synapses show complex dynamics such as rectification and voltage dependence that interact with other electrical processes in neurons. The consequences arising from these interactions for the electrical behavior of the synapse, and the dynamics they create, remain largely unexplored. Using a voltage-dependent electrical synapse between a descending modulatory projection neuron (MCN1) and a motor neuron (LG) in the crustacean stomatogastric ganglion, we find that the influence of the hyperpolarization-activated inward current (Ih) is critical to the function of the electrical synapse. When we blocked Ih with CsCl, the voltage dependence of the electrical synapse shifted by 18.7 mV to more hyperpolarized voltages, placing the dynamic range of the electrical synapse outside of the range of voltages used by the LG motor neuron (-60.2 mV to -44.9 mV). With dual electrode current- and voltage-clamp recordings, we demonstrate that this voltage shift is due to a sustained effect of Ih on the presynaptic MCN1 axon terminal membrane potential. Ih-induced depolarization of the axon terminal membrane potential increased the electrical postsynaptic potentials and currents. With Ih present, the axon terminal resting membrane potential depolarized, shifting the dynamic range of the electrical synapse towards the functional range of the motor neuron. We thus demonstrate that the function of an electrical synapse is critically influenced by a voltage-dependent ionic current (Ih).

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The resting membrane potential of Drosophila melanogaster larval muscle depends strongly on external calcium concentration

Journal of Insect Physiology ◽

10.1016/j.jinsphys.2009.11.002 ◽

2010 ◽

Vol 56 (3) ◽

pp. 304-313 ◽

Cited By ~ 5

Author(s):

Jacob L. Krans ◽

Karen D. Parfitt ◽

Kristin D. Gawera ◽

Patricia K. Rivlin ◽

Ronald R. Hoy

Keyword(s):

Drosophila Melanogaster ◽

Membrane Potential ◽

Calcium Concentration ◽

Resting Membrane Potential ◽

Larval Muscle ◽

External Calcium

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Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.3.h778 ◽

1989 ◽

Vol 257 (3) ◽

pp. H778-H784 ◽

Cited By ~ 9

Author(s):

W. P. Schilling

Keyword(s):

Endothelial Cells ◽

Membrane Potential ◽

Cytosolic Calcium ◽

Membrane Depolarization ◽

K Channel ◽

Membrane Hyperpolarization ◽

Aortic Endothelial Cells ◽

Bovine Aortic Endothelial Cells ◽

K Concentration ◽

Aortic Endothelial

The effect of bradykinin on membrane potential of cultured bovine aortic endothelial cells (BAECs) was estimated by measuring the uptake of the lipophilic cation, tetra[3H]phenylphosphonium ([3H]TPP+). Uptake of [3H]TPP+ was found to be 1) a function of extracellular K+ concentration, 2) sensitive to valinomycin, and 3) decreased by the K+ channel inhibitor, Ba2+, suggesting that the uptake of [3H]TPP+ responds to changes in membrane potential of the BAEC. Bradykinin (50 nM) produced an increase in [3H]TPP+ uptake in low K+ buffer consistent with a bradykinin-induced membrane hyperpolarization. The effect of membrane depolarization with high K+ buffer on the bradykinin-stimulated changes in cytosolic Ca2+ was determined using the fluorescent Ca2+ indicator, fura-2. The results of these experiments demonstrated that both basal cytosolic Ca2+ and bradykinin-stimulated release of Ca2+ from internal stores were not affected by membrane depolarization. However, bradykinin-stimulated influx of Ca2+ from the extracellular space decreased with membrane depolarization in a manner consistent with the movement of Ca2+ through a channel.

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Stimulation of prolactin release by dopamine withdrawal: role of membrane hyperpolarization

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1994.267.5.e781 ◽

1994 ◽

Vol 267 (5) ◽

pp. E781-E788 ◽

Cited By ~ 3

Author(s):

K. A. Gregerson ◽

N. Golesorkhi ◽

R. Chuknyiska

Keyword(s):

Resting Membrane Potential ◽

Prolactin Release ◽

Membrane Hyperpolarization ◽

Basal Release ◽

K Concentration ◽

Hypothalamic Dopamine ◽

Ca2 Channels ◽

Stimulation Of ◽

External K

Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland, whereas removal of DA markedly augments its release to values exceeding pre-DA rates. We investigated whether electrical events induced by DA contribute to this secretory rebound. In primary cultured lactotropes, spontaneous Ca(2+)-dependent spiking activity was enhanced after recovery from DA-induced hyperpolarization. Voltage clamp studies showed a rapidly and a slowly inactivating Ca2+ current that were both augmented by a hyperpolarizing conditioning potential. We measured PRL release from perifused cells exposed to DA to correlate the electrical with the secretory responses. DA inhibited PRL release by 67%, whereas PRL secretion increased three- to fourfold over basal release after washout of DA. Valinomycin, used to directly hyperpolarize the cell membrane, mimicked the actions of DA, inhibiting PRL release (65%) and, upon washout, augmenting PRL secretion. Blocking the DA- or valinomycin-induced hyperpolarization by elevating external K+ concentration blocked both the inhibition and rebound of PRL release. These novel results demonstrate that hyperpolarization of the lactotrope membrane by DA is critical for the development of PRL rebound after DA withdrawal. We hypothesize the mechanism involves the removal of inactivation from a population of Ca2+ channels, leading to enhanced Ca2+ influx and PRL release upon recovery of the resting membrane potential after DA removal.

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Ca(2+)-induced inhibition of 45Ca2+ influx and Ca2+ current in smooth muscle of the rat vas deferens

AJP Cell Physiology ◽

10.1152/ajpcell.1996.270.5.c1468 ◽

1996 ◽

Vol 270 (5) ◽

pp. C1468-C1477 ◽

Cited By ~ 7

Author(s):

M. A. Khoyi ◽

T. Ishikawa ◽

K. D. Keef ◽

D. P. Westfall

Keyword(s):

Vas Deferens ◽

Rat Vas Deferens ◽

Inhibitory Effects ◽

Isolated Cells ◽

Inositol 1,4,5 Trisphosphate ◽

Voltage Dependent ◽

Steady State Inactivation ◽

Inward Currents ◽

K Concentration ◽

Ca2 Channels

The present study investigates how changes in intracellular Ca2+ concentration modulate the influx of 45Ca2+ in isolated rat vasa deferentia. Raising extracellular K+ concentration ([K+]0) to > or = 32 mM increased 45Ca2+ influx during the 1st min in solutions containing 0.03-1.5 mM extracellular Ca2+ concentration ([Ca2+]0). During the 6th min in [K+]0 > or = 50 mM, 45Ca2+ influx was less than during the 1st min. This decline in 45Ca2+ influx occurred for [Ca2+]0 > or = 0.4 mM. Procaine potentiated K(+)-stimulated 45Ca2+ influx in 1.5 mM [Ca2+]0 and eliminated the decline of 45Ca2+ influx in low [Ca2-]0. Ryanodine and norepinephrine reduced K(+)-stimulated 45Ca2+ influx. 45Ca2+ content changed with time in accordance with the changes observed in 45Ca2+ influx. In isolated cells, voltage-dependent inward currents inactivated more rapidly with 1.5 mM Ca2+ as the charge carrier than with 1.5 mM Ba2+, and the steady-state inactivation relationship was shifted in the hyperpolarizing direction. Inward current was reduced with either caffeine, ryanodine, or norepinephrine. The inhibitory effects of norepinephrine were abolished by depletion of intracellular Ca2+ stores. These results are compatible with the hypothesis that K(+)-stimulated 45Ca2+ influx declines with time due to Ca(2+)-induced inhibition of Ca2- channels. Ca(2+)- and inositol 1,4,5-trisphosphate-induced releases of Ca2+ from the sarcoplasmic reticulum appear to play an important role in this process.

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