Membrane resistance increases when automaticity develops in explanted rat heart cells

1990 ◽  
Vol 258 (1) ◽  
pp. H145-H152 ◽  
Author(s):  
O. F. Schanne ◽  
M. Lefloch ◽  
B. Fermini ◽  
E. Ruiz-Petrich
Keyword(s):  
Spontaneous Activity ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Heart Cells ◽  
Membrane Capacity ◽  
Rat Heart Cells ◽  
Specific Membrane

We compared the passive electrical properties of isolated ventricular myocytes (resting potential -65 mV, fast action potentials, and no spontaneous activity) with those of 2- to 7-day-old cultured ventricle cells from neonatal rats (resting potential -50 mV, slow action potentials, and presence of spontaneous activity). In myocytes the specific membrane capacity was 0.99 microF/cm2, and the specific membrane resistance increased from 2.46 k omega.cm2 at -65 mV to 7.30 k omega.cm2 at -30 mV. In clusters, the current-voltage relationships measured under current-clamp conditions showed anomalous rectification and the input resistance decreased from 1.05 to 0.48 M omega when external K+ concentration was increased from 6 to 100 mM. Using the model of a finite disk we determined the specific membrane resistance (12.9 k omega.cm2), the effective membrane capacity (17.8 microF/cm2), and the lumped resistivity of the disk interior (1,964 omega.cm). We conclude that 1) the voltage dependence of the specific membrane resistance cannot completely explain the membrane resistance increase that accompanies the appearance of spontaneous activity; 2) a decrease of the inwardly rectifying conductance (gk1) is mainly responsible for the increase in the specific membrane resistance and depolarization; and 3) approximately 41% of the inward-rectifying channels are electrically silent when spontaneous activity develops in explanted ventricle cells.

Properties of visceral primary afferent neurons in the nodose ganglion of the rabbit

1985 ◽  
Vol 54 (2) ◽  
pp. 245-260 ◽  
Author(s):  
C. E. Stansfeld ◽  
D. I. Wallis
Keyword(s):  
Action Potentials ◽  
Input Resistance ◽  
Nodose Ganglion ◽  
Time Dependent ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
C Cells ◽  
Axonal Conduction ◽  
A Cells

The active and passive membrane properties of rabbit nodose ganglion cells and their responsiveness to depolarizing agents have been examined in vitro. Neurons with an axonal conduction velocity of less than 3 m/s were classified as C-cells and the remainder as A-cells. Mean axonal conduction velocities of A- and C-cells were 16.4 m/s and 0.99 m/s, respectively. A-cells had action potentials of brief duration (1.16 ms), high rate of rise (385 V/s), an overshoot of 23 mV, and relatively high spike following frequency (SFF). C-cells typically had action potentials with a "humped" configuration (duration 2.51 ms), lower rate of rise (255 V/s), an overshoot of 28.6 mV, an after potential of longer duration than A-cells, and relatively low SFF. Eight of 15 A-cells whose axons conducted at less than 10 m/s had action potentials of longer duration with a humped configuration; these were termed Ah-cells. They formed about 10% of cells whose axons conducted above 2.5 m/s. The soma action potential of A-cells was blocked by tetrodotoxin (TTX), but that of 6/11 C-cells was unaffected by TTX. Typically, A-cells showed strong delayed (outward) rectification on passage of depolarizing current through the soma membrane and time-dependent (inward) rectification on inward current passage. Input resistance was thus highly sensitive to membrane potential close to rest. In C-cells, delayed rectification was not marked, and slight time-dependent rectification occurred in only 3 of 25 cells; I/V curves were normally linear over the range: resting potential to 40 mV more negative. Data on Ah-cells were incomplete, but in our sample of eight cells time-dependent rectification was absent or mild. C-cells had a higher input resistance and a higher neuronal capacitance than A-cells. In a proportion of A-cells, RN was low at resting potential (5 M omega) but increased as the membrane was hyperpolarized by a few millivolts. A-cells were depolarized by GABA but were normally unaffected by 5-HT or DMPP. C-cells were depolarized by GABA in a similar manner to A-cells but also responded strongly to 5-HT; 53/66 gave a depolarizing response, and 3/66, a hyperpolarizing response. Of C-cells, 75% gave a depolarizing response to DMPP.(ABSTRACT TRUNCATED AT 400 WORDS)

Electrical and Mechanical Properties of the Red and White Muscles in the Silver Carp

1972 ◽  
Vol 57 (2) ◽  
pp. 551-567
Author(s):  
T. YAMAMOTO
Keyword(s):  
Mechanical Properties ◽  
White Muscle ◽  
Silver Carp ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Mechanical Responses ◽  
Red Muscle ◽  
Red And White Muscles ◽  
Specific Membrane

1. Electrical and mechanical properties of the red muscle (M. levator pinnae pectoralis) and white muscle (M. levator pinnae lateralis abdominis) in the silver carp (Carassius auratus Linné) were investigated by using caffeine and thymol. 2. A complete tetanus could be produced in the red muscle. But in the white muscle no tetanus was produced and there was a gradual decrease in tension during continuous stimulation, even at a frequency of 1 c/s or less. 3. Caffeine (0.5-1 mM) and thymol (0.25-0.5 mM) potentiated the twitch tension in both muscles without an increase in the resting tension; they produced a contracture in both muscles when the concentration was increased further. 4. The falling phase of the active state of contraction was nearly the same in both muscles and was prolonged by caffeine (0.5 mmM) and by thymol (0.25 mM). 5. The resting membrane potential of the red muscle was scarcely affected by caffeine (0.5-5 mM), whereas in the white muscles a depolarization of 10 mV was observed with caffeine of more than 2 mM. The resting potential of both muscles was little changed by o.25 mm thymol. However, at a concentration of more than 0.5mM thymol depolarized the membrane in both muscles to the same extent. 6. In caffeine (2-3 mM) solution the mean specific membrane resistance was reduced from 8.8 kΩ cm2 to 6.0 kΩ cm2 in the red muscle, and from 5.0 kΩ cm2 to 2.7 kΩ cm2 in the white muscle. In thymol (0.5-1 mM) solution it was reduced from 11.2 kΩcm2 to 6.5 kΩ cm2 in the red muscle, and from 5.4kΩ cm2 to 3.1 kΩ) cm2 in the white muscle. The specific membrane capacitance, calculated from the time constant and the membrane resistance, remained more or less the same in both muscles after a treatment with these agents. 7. Electrical properties of the muscles and the effects of caffeine and thymol on mechanical responses suggest that there are no fundamental differences between red and white muscles except for the excitation-contraction coupling. A lack of summation of twitch, a successive decline of twitch, and inability to produce potassium contracture in the white muscle may be due to the fact that the Ca-releasing mechanism is easily inactivated by depolarization of the membrane.

scholarly journals Ability of the orally effective iron chelators dimethyl- and diethyl- hydroxypyrid-4-one and of deferoxamine to restore sarcolemmal thiolic enzyme activity in iron-loaded heart cells

Blood ◽  
1994 ◽  
Vol 83 (9) ◽  
pp. 2692-2697 ◽  
Author(s):  
G Link ◽  
A Pinson ◽  
C Hershko
Keyword(s):  
Enzyme Activity ◽  
Iron Chelation ◽  
Myocardial Cell ◽  
Resting Potential ◽  
Molar Ratio ◽  
Iron Chelators ◽  
Heart Cell ◽  
Heart Cells ◽  
Cell Organelles ◽  
Rat Heart Cells

In view of the profound functional and structural abnormalities shown in our previous studies in cultured, iron-loaded rat heart cells, we have examined the ability of the orally effective iron chelators dimethyl-3-hydroxypyrid-4-one (DMHP or L1) and diethyl-3-hydroxy-pyrid- 4-one (DEHP or CP94) and of deferoxamine (DF) to reverse the damage caused by iron loading to heart cell organelles. At a concentration of 1.0 mmol/L, all three iron chelators were equally efficient in removing iron and restoring the activity of the thiolic sarcolemmal enzymes 5′- nucleotidase and Na,K,ATPase. However, at 0.1 mmol/L DMHP and DEHP were less effective than DF both in their iron-mobilizing effect and in promoting thiolic enzyme recovery. The superior efficiency of DF at low concentrations illustrates the advantage of the hexadentate chelating action of DF as compared with bidentate chelators such as DMHP and DEHP requiring a 3 to 1 molar ratio to iron for optimal effect. In contrast to its beneficial effect on sarcolemmal enzyme activity, iron chelation was unable to reverse the increase in beta-hexosaminidase activity caused by abnormal lysosomal fragility. Our study demonstrates for the first time that iron-induced peroxidative damage to the myocardial cell is associated with a marked loss of Na,K,ATPase activity, an enzyme with a major role in the maintenance of cellular resting potential. The timing of this damage and the restoration of Na,K,ATPase function by iron-chelating treatment suggest a cause-and-effect relationship between the observed injury to the sarcolemmal enzyme and the reversible electrophysiologic abnormalities observed in the same heart culture system in our previous studies.

Classes of Light-Evoked Response in the Retina of Strombus

1979 ◽  
Vol 80 (1) ◽  
pp. 287-297
Author(s):  
FREDERICK N. QUANDT ◽  
HOWARD L. GILLARY
Keyword(s):  
Optic Nerve ◽  
Action Potentials ◽  
Input Resistance ◽  
Resting Potential ◽  
Recording Site ◽  
Charging Time ◽  
Rate Of Decay ◽  
Hyperpolarizing Response ◽  
Strombus Luhuanus ◽  
A Site

Two general classes of light-evoked responses were recorded intracellularly from the retina of Strombus luhuanus. In one class, retinal illumination caused depolarization, the amplitude of which was graded with light intensity. In the other, it produced hyperpolarization and concomitant inhibition of repetitive action potentials. There were two types of depolarizing waveform. Each was associated with a different type of intraccllular recording site, characterized on the basis of electrical properties in the dark. In general, the type of response with a more rapid rate of decay was recorded from a site which exhibited a lower resting potential, higher input resistance, and longer ‘membrane charging time.’ The two depolarizing responses and the hyperpolarizing response apparently each arose from a different type of neurone. The depolarizing types, at least one of which is a photoreceptor, apparently give rise to the cornea-negativity of the electroretinogram and ‘on’ activity in the optic nerve fibres. The hyperpolarizing type apparently mediates ‘off’ activity in the optic nerve.

Effects of Octopamine on Calcium Action Potentials in Insect Oocytes

1989 ◽  
Vol 142 (1) ◽  
pp. 115-124
Author(s):  
M. J. O'DONNELL ◽  
B. SINGH
Keyword(s):  
Action Potentials ◽  
Rank Order ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Threshold Concentration ◽  
Resting Potential ◽  
Calcium Dependent ◽  
Octopamine Receptors ◽  
Voltage Dependent ◽  
Maximum Rate Of Rise

Our experiments show that octopamine receptors are present on the developing follicles of an insect, Rhodnius prolixus. Application of D,L-octopamine decreased the duration and overshoot of calcium-dependent action potentials (APs), and increased the intrafollicular concentration of cyclic AMP. The threshold concentration of D,L-octopamine for the reduction in electrical excitability was between 1 and 5×10−7moll−1, and maximal effects of a 40–50% reduction in AP overshoot and duration were apparent at 10−4moll−1. At concentrations above 10−5moll−1, a small (<10%) hyperpolarization of the resting potential was also apparent. Effects of D,L-octopamine on oocyte excitability were independent of these small shifts in resting potential. Current injection experiments, in which calcium entry was blocked by cobalt, demonstrated that D,L-octopamine reduced membrane resistance at both hyperpolarizing and depolarizing potentials. Octopamine did not affect the maximum rate of rise of the AP, dV/dtmax, which is an indicator of inward calcium current. It is suggested that octopamine may mediate its effects on excitability through an increase in a voltage-dependent potassium conductance. Application of other phenolamines indicated a rank order of potency of D, Loctopamine > D,L-synephrine > tyramine. The α-adrenergic agonists clonidine, naphazoline and tolazoline were without significant effect at 10−5-10−3moll−1. Reduction of excitability by D,L-octopamine was effectively blocked by phentolamine and metoclopramide. Yohimbine and gramine were less effective as antagonists. Possible functions of octopamine receptors in insect follicles are discussed.

Myosin heavy chain turnover in cultured neonatal rat heart cells: effects of [Ca2+]i and contractile activity

1996 ◽  
Vol 271 (5) ◽  
pp. C1447-C1456 ◽  
Author(s):  
K. L. Byron ◽  
J. L. Puglisi ◽  
J. R. Holda ◽  
D. Eble ◽  
A. M. Samarel
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Protein Turnover ◽  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Myofibrillar Protein ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Cell Shortening ◽  
Rat Heart Cells

Blockade of L-type Ca2+ channels in spontaneously contracting cultured neonatal rat ventricular myocytes causes contractile arrest, myofibrillar disassembly, and accelerated myofibrillar protein turnover. To determine whether myofibrillar protein turnover. To determine whether myofibrillar atrophy results indirectly from loss of mechanical signals or directly from alterations in intracellular Ca2+ concentration ([Ca2+]i), contractile activity was inhibited with verapamil (10 microM) or 2,3-butanedione monoxime (BDM), and their effects on cell shortening, [Ca2+]i, and myosin heavy chain (MHC) turnover were assessed. Control cells demonstrated spontaneous [Ca2+]i transients (peak amplitude 232 +/- 15 nM, 1-2 Hz) and vigorous contractile activity. Verapamil inhibited shortening by eliminating spontaneous [Ca2+]i transients. Low concentrations of BDM (5.0-7.5 mM) had no effect on basal or peak [Ca2+]i transient amplitude but reduced cell shortening, whereas 10 mM BDM reduced both [Ca2+]i transient amplitude and shortening. Both agents inhibited MHC synthesis, but only verapamil accelerated MHC degradation. Thus MHC half-life does not change in parallel with contractile activity but rather more closely follows changes in [Ca2+]i. [Ca2+]i transients appear critical in maintaining myofibrillar assembly and preventing accelerated MHC proteolysis.

Electrotonic suppression of early afterdepolarizations in isolated rabbit Purkinje myocytes

2000 ◽  
Vol 279 (1) ◽  
pp. H250-H259 ◽  
Author(s):  
Delilah J. Huelsing ◽  
Kenneth W. Spitzer ◽  
Andrew E. Pollard
Keyword(s):  
Ventricular Myocytes ◽  
Single Cells ◽  
Late Phase ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Early Afterdepolarizations ◽  
Model Cell ◽  
Triggered Arrhythmias ◽  
Electrotonic Interactions ◽  
Coupling Current

Many studies suggest that early afterdepolarizations (EADs) arising from Purkinje fibers initiate triggered arrhythmias under pathological conditions. However, electrotonic interactions between Purkinje and ventricular myocytes may either facilitate or suppress EAD formation at the Purkinje-ventricular interface. To determine conditions that facilitated or suppressed EADs during Purkinje-ventricular interactions, we coupled single Purkinje myocytes and aggregates isolated from rabbit hearts to a passive model cell via an electronic circuit with junctional resistance ( R j). The model cell had input resistance ( R m,v) of 50 MΩ, capacitance of 39 pF, and a variable rest potential ( V rest,v). EADs were induced in Purkinje myocytes during superfusion with 1 μM isoproterenol. Coupling at high R j to normally polarized V rest,v established a repolarizing coupling current during all phases of the Purkinje action potential. This coupling current preferentially suppressed EADs in single cells with mean membrane resistance ( R m,p) of 297 MΩ, whereas EAD suppression in larger aggregates with mean R m,p of 80 MΩ required larger coupling currents. In contrast, coupling to elevated V rest,v established a depolarizing coupling current during late phase 2, phase 3, and phase 4 that facilitated EAD formation and induced spontaneous activity in single Purkinje myocytes and aggregates. These results have important implications for arrhythmogenesis in the infarcted heart when reduction of the ventricular mass due to scarring alters the R m,p-to- R m,v ratio and in the ischemic heart when injury currents are established during coupling between polarized Purkinje myocytes and depolarized ventricular myocytes.

Posttetanic hyperpolarization produced by electrogenic Na(+)-K+ pump in lizard axons impaled near their motor terminals

1993 ◽  
Vol 70 (5) ◽  
pp. 1874-1884 ◽  
Author(s):  
K. Morita ◽  
G. David ◽  
J. N. Barrett ◽  
E. F. Barrett
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Input Resistance ◽  
Peak Amplitude ◽  
Resting Potential ◽  
Tetanic Stimulation ◽  
Train Duration ◽  
Consistent Change ◽  
Nodal Voltage

1. The hyperpolarization that follows tetanic stimulation was recorded intra-axonally from the internodal region of intramuscular myelinated motor axons. 2. The peak amplitude of the posttetanic hyperpolarization (PTH) that followed stimulation at 20-100 Hz for < or = 35 s increased with increasing train duration, reaching a maximum of 22 mV. PTH decayed over a time course that increased from tens to hundreds of seconds with increasing train duration. For a given frequency of stimulation the time integral of PTH was proportional to the number of stimuli in the train, averaging 3-4 mV.s per action potential. 3. Ouabain (0.1-1 mM) and cyanide (1 mM) depolarized the resting potential and abolished PTH. Tetanic stimulation in ouabain was followed by a slowly decaying depolarization (probably due to extra-axonal K+ accumulation) whose magnitude and duration increased as the duration of the train increased. 4. Axonal input resistance showed no consistent change during PTH in normal solution but increased during PTH in the presence of 3 mM Cs+ (which blocks axonal inward rectifier currents). 5. PTH was abolished when bath Na+ was replaced by Li+ or choline. PTH persisted after removal of bath Ca2+ and addition of 2 mM Mn2+. 6. Removal of bath K+ abolished the PTH recorded after brief stimulus trains and greatly reduced the duration of PTH recorded after longer stimulus trains. 7. A brief application of 10 mM K+, which normally depolarizes axons, produced a ouabain-sensitive hyperpolarization in axons bathed in K(+)-free solution. 8. These observations suggest that in these myelinated axons PTH is produced mainly by activation of an electrogenic Na(+)-K(+)-ATPase, rather than by changes in K+ permeability or transmembrane [K+] gradients. This conclusion is supported by calculations showing agreement between estimates of Na+ efflux/impulse based on PTH measurements and estimates of Na+ influx/impulse based on nodal voltage-clamp measurements. Pump activity also appears to contribute to the resting potential. 9. The stimulus intensity required to initiate a propagating action potential increased during PTH but decreased during the posttetanic depolarization recorded in ouabain. Thus changes in axonal excitability after tetanic stimulation correlate with changes in the posttetanic membrane potential. 10. Action potentials that propagated during PTH had a larger peak amplitude and were followed by a larger and longer depolarizing afterpotential than action potentials elicited at the resting potential. This enhancement of the depolarizing afterpotential is consistent with previous reports of an increased superexcitable period after action potentials evoked during PTH.

Electrophysiological characterization of single pregnant rat myometrial cells in short-term primary culture

1986 ◽  
Vol 250 (1) ◽  
pp. C47-C54 ◽  
Author(s):  
P. Mollard ◽  
J. Mironneau ◽  
T. Amedee ◽  
C. Mironneau
Keyword(s):  
Action Potential ◽  
Primary Culture ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Short Term ◽  
Pregnant Rat ◽  
Myometrial Cells ◽  
The Mean ◽  
Electrophysiological Characterization ◽  
Specific Membrane

Smooth muscle cells were isolated from the longitudinal layer of pregnant rat myometrium (18-19 days) and studied either freshly dissociated or during short-term primary culture (until 30 h) using intracellular microelectrode techniques and direct microscopic observation. The isolated myometrial cells excluded trypan blue vital stain and could repetitively contract in response to various stimuli. Electrophysiological studies at 37 degrees C showed normal resting potential (-54.5 +/- 7.5 mV, n = 71). Action potentials with overshoot (+7.8 +/- 4.6 mV, n = 71) could be elicited by intracellular stimulation. Moreover, the membrane potential was largely dependent on the external K+ concentration. The action potential was suppressed in a Ca2+-free solution [with 0.1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid], and the overshoot amplitude was clearly Ca2+ dependent. The action potential was inhibited by Mn2+ ions (1 mM), Co2+ ions (1 mM), and D 600 (1 microM) but was unaffected by tetrodotoxin (2 microM) and external Na+ removal. Tetraethylammonium chloride (TEA, 10 mM) and 4-aminopyridine (4-AP, 10 mM) increased both overshoot amplitude and duration of the electrical responses. When the cell surface area was measured with light microscopy, the mean specific membrane resistance was 14.8 +/- 4.6 k omega . cm2 (n = 14), and the mean specific membrane capacitance was 2.3 +/- 0.7 microF/cm2 (n = 14). Outward-going rectification was consistently observed in all cells examined. This was either inhibited by TEA and 4-AP (10 mM each) or reduced in the presence of 1 mM Mn2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Passive properties of the membrane of single freshly isolated smooth muscle cells

1980 ◽  
Vol 239 (5) ◽  
pp. C153-C161 ◽  
Author(s):  
J. J. Singer ◽  
J. V. Walsh
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Stable Steady State ◽  
Membrane Area ◽  
Ion Substitution ◽  
Length Constant

Single, smooth muscle cells were isolated from the stomach muscularis of the toad Bufo marinus and studied on the same day as isolation using standard electrophysiological techniques and direct microscopic observation at high magnification. Following penetration a period of hyperpolarization occurred that appeared to be caused by an increase in K+ conductance activated by Ca2+ entering the cell upon penetration. Ion substitution studies showed that the stable steady-state resting potential was dependent on both [Na+]0 and [K+]0. At [Ca2+]0 = 1.8 mM, active responses could be elicited which, at the higher [Ca2+]0 (< 8mM) generally employed, became action potentials with overshoots. Calculations employing the equations for a short cable and the observed change of membrane potential as a single exponential in response to a small hyperpolarizing current step both indicated that the length constant (lambda) was sufficiently greater than the cell length so that the cell behaved as an isopotential surface during subthreshold perturbations. From photomicrographic measurements of each cell studied and the input resistance, values of specific membrane resistance (Rm) were obtained that ranged as high as 152 k omega x cm2 depending on the ionic environment, most notably on [Ca2+]0. The membrane capacity (Cm) referred to the surface area measured with light microscopy was 1.3 +/- 0.3 microF/cm2 (mean +/- SD). When the best estimate of caveolar membrane area was included, Cm referred to total membrane area (caveolar plus noncaveolar) was approximately 0.8 microF/cm2.

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