Endurance training alters outward K+current characteristics in rat cardiocytes

2001 ◽  
Vol 90 (4) ◽  
pp. 1327-1333 ◽  
Author(s):  
Korinne N. Jew ◽  
M. Charlotte Olsson ◽  
Eric A. Mokelke ◽  
Bradley M. Palmer ◽  
Russell L. Moore
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Primary Culture ◽  
Left Ventricular ◽  
Resting Membrane Potential ◽  
Sprague Dawley ◽  
Whole Cell ◽  
Time To Peak ◽  
Time Required ◽  
In Cells

The effect of endurance run training on outward K+ currents with rapidly inactivating ( I to) and sustained or slowly inactivating ( I sus) characteristics was examined in left ventricular (LV) cardiocytes isolated from sedentary (Sed) and treadmill-trained (Tr) female Sprague-Dawley rats. Isolated LV cardiocytes were used in whole cell patch-clamp studies to characterize whole cell I to and I sus. Peak I to was greatest in cells isolated from the Tr group. When I to was corrected for cell capacitance to yield a current density, most, but not all, of the Sed vs. Tr differences in I to magnitude were eliminated. Regardless of how I to was expressed (e.g., I to or I todensity), the time required to achieve a peak value was markedly shortened in the cardiocytes isolated from the Tr group. Training elicited a reduction in I sus density. Action potential characteristics were determined in Sed and Tr cardiocytes in primary culture. Training did not affect resting membrane potential, whereas peak membrane potential was reduced and time to peak membrane potential was prolonged in the Tr group. In addition, time to 50% repolarization was significantly increased in cells from the Tr group. Collectively, these data indicate that I to and I sus characteristics are altered by training in isolated LV cardiocytes. These alterations in I to and I sus may be responsible, at least in part, for the training-induced alterations in action potential configuration in cardiocytes in primary culture.

Influence of age and run training on cardiac Na+/Ca2+ exchange

2003 ◽  
Vol 95 (5) ◽  
pp. 1994-2003 ◽  
Author(s):  
Lisa C. Mace ◽  
Bradley M. Palmer ◽  
David A. Brown ◽  
Korinne N. Jew ◽  
Joshua M. Lynch ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Left Ventricular ◽  
Brown Norway ◽  
Resting Membrane Potential ◽  
Whole Cell Patch Clamp ◽  
Age Related ◽  
Intracellular Ca ◽  
Whole Heart ◽  
Exchange Activity

Effects of age and training on myocardial Na+/Ca2+ exchange were examined in young sedentary (YS; 14-15 mo), aged sedentary (AS; 27-31 mo), and aged trained (AT; 8- to 11-wk treadmill run training) male Fischer Brown Norway rats. Whole heart performance and isolated cardiocyte Na+/Ca2+ exchange characteristics were measured. At the whole heart level, a small but significant slowing of late isovolumic left ventricular (LV) relaxation, which may be indicative of altered Na+/Ca2+ exchange activity, was seen in hearts from AS rats. This subtle impairment in relaxation was not observed in hearts from AT rats. At the single-cardiocyte level, late action potential duration was prolonged, resting membrane potential was more positive, and overshoot potential was greater in cardiocytes from AS rats than from YS rats ( P < 0.05). Training did not influence any of these age-related action potential characteristics. In electrically paced cardiocytes, neither shortening nor intracellular Ca2+ concentration ([Ca2+]i) dynamics was influenced by age or training. Similarly, neither age nor training influenced the rate of [Ca2+]i clearance via forward (Nain+ /Caout2+) Na+/Ca2+ exchange after caffeine-induced Ca2+ release from the sarcoplasmic reticulum or cardiac Na+/Ca2+ exchanger protein (NCX1) expression. However, when whole cell patch-clamp techniques combined with fluorescence microscopy were used to evaluate the ability of Na+/Ca2+ exchange to alter cytosolic [Ca2+] ([Ca2+]c) under conditions where membrane potential ( Vm) and internal and external [Na+] and [Ca2+] could be controlled, we observed age-associated increases in forward Na+/Ca2+ exchange-mediated [Ca2+]c clearance ( P < 0.05) that were not influenced by training. The age-related increase in forward Na+/Ca2+ exchange activity provides a hypothetical explanation for the late action potential prolongation observed in this study.

Temperature dependence of electrophysiological properties of guinea pig and ground squirrel myocytes

1992 ◽  
Vol 263 (1) ◽  
pp. R177-R184 ◽  
Author(s):  
J. C. Herve ◽  
K. Yamaoka ◽  
V. W. Twist ◽  
T. Powell ◽  
J. C. Ellory ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Action Potential ◽  
Ground Squirrel ◽  
Calcium Release ◽  
Maximum Amplitude ◽  
Calcium Currents ◽  
Resting Membrane Potential ◽  
Electrophysiological Properties ◽  
Time To Peak

The effects of changing temperature on the electrophysiology of isolated cardiac myocytes of the guinea pig and Richardson's ground squirrel were studied by patch-clamp techniques. In cells from both species, the resting membrane potential declined on cooling from 36 to 12 degrees C by approximately 6 mV. The duration of the plateau of the action potential in guinea pig cells increased monotonically on cooling. In contrast, the action potential of ground squirrel cells showed a biphasic response, increasing in duration from 36 to 24 degrees C and then decreasing on cooling from 24 to 12 degrees C. From voltage-clamp studies, the properties of L-type calcium currents (ICa) on cooling were compared in the two species and were found to be similar: In both cases, ICa decreased in amplitude from approximately 2 nA peak current at 36 degrees C to less than 400 pA at 12 degrees C. The Q10 of both the maximum amplitude and time to peak for ICa in both species was approximately 1.8. The time for half inactivation had a greater Q10 of 2.5-3. It is concluded that, surprisingly, factors affecting the resting membrane potential and properties of L-type calcium channels are not major contributors to cardiac dysfunction on cooling. Rather, it is sarcoplasmic reticulum calcium release and reuptake that are likely to be the most important cold-sensitive processes.

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

2007 ◽  
Vol 292 (1) ◽  
pp. R388-R395 ◽  
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.

Exposure to low temperature prepares the turtle brain to withstand anoxic environments during overwintering

2021 ◽  
Author(s):  
Ebrahim Lari ◽  
Leslie T. Buck
Keyword(s):  
Membrane Potential ◽  
Low Temperature ◽  
Action Potential ◽  
Pyramidal Neurons ◽  
Cellular Damage ◽  
Severe Hypoxia ◽  
Painted Turtle ◽  
Whole Cell ◽  
Voltage Gated ◽  
The Impact

In most vertebrates, anoxia drastically reduces the production of the essential adenosine triphosphate (ATP) to power its many necessary functions, and consequently, cell death occurs within minutes. However, some vertebrates, such as the painted turtle (Chrysemys picta bellii), have evolved the ability to survive months without oxygen by simultaneously decreasing ATP supply and demand, surviving the anoxic period without any apparent cellular damage. The impact of anoxia on the metabolic function of painted turtles has received a lot of attention. Still, the impact of low temperature has received less attention and the interactive effect of anoxia and temperature even less. In the present study, we investigated the interactive impacts of reduced temperature and severe hypoxia on the electrophysiological properties of pyramidal neurons in painted turtle cerebral cortex. Our results show that an acute reduction in temperature from 20 to 5°C decreases membrane potential, action potential width and amplitude, and whole-cell conductance. Importantly, acute exposure to 5°C considerably slows membrane repolarization by voltage-gated K+ channels. Exposing pyramidal cells to severe hypoxia in addition to an acute temperature change slightly depolarized membrane potential but did not alter action potential amplitude or width and whole-cell conductance. These results suggest that acclimation to low temperatures, preceding severe environmental hypoxia, induces cellular responses in pyramidal neurons that facilitate survival under low oxygen concentration. In particular, our results show that temperature acclimation invokes a change in voltage-gated K+ channel kinetics that overcomes the acute inhibition of the channel.

Hypertensive-diabetic cardiomyopathy in rats

1990 ◽  
Vol 258 (3) ◽  
pp. H793-H805 ◽  
Author(s):  
F. S. Fein ◽  
B. E. Zola ◽  
A. Malhotra ◽  
S. Cho ◽  
S. M. Factor ◽  
...  
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Action Potential Duration ◽  
Stimulus Frequency ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Resting Membrane Potential ◽  
Contraction And Relaxation ◽  
And Control ◽  
Myocardial Pathology

Left ventricular papillary muscle function, transmembrane action potentials, myosin adenosinetriphosphatase (ATPase) and isoenzyme distribution, and myocardial pathology were studied in hypertensive (H), diabetic (D), hypertensive-diabetic (HD), and control (C) rats. There was approximately 50% relative left ventricular hypertrophy in H and HD rats. Relative lung and liver weights were greater in HD rats. Peak velocity of shortening tended to decrease progressively in H, D, and HD rats. The duration of contraction and relaxation was markedly prolonged in Ds and HDs. The length-developed tension relation was blunted in HDs. The negative inotropic effect of verapamil was similar in all groups. Resting membrane potential and amplitude were decreased in D and HD rats. Action potential duration was increased in H, D, and especially HD rats. The shortening of action potential duration with increased stimulus frequency was greater in H, D, and especially HD rats than in Cs. Left ventricular myosin ATPase and V1 isoenzyme content decreased progressively in H, D, and HD rats. Right ventricular V1 isoenzyme content was not affected in H rats but was markedly decreased in D and HD rats. Left (and right) ventricular pathology was unchanged in rats with diabetes but was increased in rats with hypertension. These data suggest that the combination of myocardial pathology (due to hypertension) and cellular dysfunction (caused mainly by diabetes) may result in cardiomyopathy and congestive heart failure in the HD rat.

Hormonal Signaling Actions on Kv7.1 (KCNQ1) Channels

2021 ◽  
Vol 61 (1) ◽  
pp. 381-400
Author(s):  
Emely Thompson ◽  
Jodene Eldstrom ◽  
David Fedida
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cardiac Action Potential ◽  
Resting Membrane Potential ◽  
Voltage Gated ◽  
M Current ◽  
Kv7 Channels ◽  
Cardiac Action ◽  
Repolarization Phase ◽  
And Control

Kv7 channels (Kv7.1–7.5) are voltage-gated K+ channels that can be modulated by five β-subunits (KCNE1–5). Kv7.1-KCNE1 channels produce the slow-delayed rectifying K+ current, IKs, which is important during the repolarization phase of the cardiac action potential. Kv7.2–7.5 are predominantly neuronally expressed and constitute the muscarinic M-current and control the resting membrane potential in neurons. Kv7.1 produces drastically different currents as a result of modulation by KCNE subunits. This flexibility allows the Kv7.1 channel to have many roles depending on location and assembly partners. The pharmacological sensitivity of Kv7.1 channels differs from that of Kv7.2–7.5 and is largely dependent upon the number of β-subunits present in the channel complex. As a result, the development of pharmaceuticals targeting Kv7.1 is problematic. This review discusses the roles and the mechanisms by which different signaling pathways affect Kv7.1 and KCNE channels and could potentially provide different ways of targeting the channel.

Effect of cold temperature on membrane potential responses in opossum esophageal circular muscle

1989 ◽  
Vol 257 (4) ◽  
pp. G637-G643
Author(s):  
D. Kauvar ◽  
J. Crist ◽  
R. K. Goyal
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Cold Temperature ◽  
Resting Membrane Potential ◽  
Spike Potential ◽  
Circular Smooth Muscle ◽  
Time To Peak ◽  
Proximal Site

The effects of cold temperature on resting membrane potential (RMP) and membrane potential responses to depolarizing electrical current and intramural nerve stimulation were examined in opossum esophageal circular smooth muscle. Intracellular recordings were made in smooth muscle strips obtained from 7 to 8 cm (proximal site) and 1 to 2 cm (distal site) above the lower esophageal sphincter. RMP was not affected by changes in temperature between 34 and 22 degrees C. Cooling caused progressive inhibition of the amplitude and a slight increase in the duration of the spike potential produced by depolarizing current. Cooling did not modify the threshold for spike potential generation but decreased the spike amplitude from 34.0 +/- 0.5 mV at 34 degrees C to 14.1 +/- 2.2 mV at 22 degrees C (P less than 0.01). Electrical field stimulation with single electrical pulses (1.0 ms) produced tetrodotoxin-sensitive biphasic membrane responses consisting of initial hyperpolarization, or an inhibitory junction potential followed by depolarization that increased in amplitude as temperature was decreased from 34 to 26 degrees C and then decreased in amplitude as temperature was further decreased. At both proximal and distal sites cooling from 34 to 22 degrees C caused more than a twofold increase in the duration of hyperpolarization and time to peak depolarization. However, the increase in the absolute time of the duration of hyperpolarization and the time to peak depolarization was significantly greater at the distal than proximal esophageal site. Cooling to 16 degrees C decreased RMP and nearly abolished the biphasic membrane potential response.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sodium on beta-cell electrical activity

1982 ◽  
Vol 242 (5) ◽  
pp. C296-C303 ◽  
Author(s):  
B. Ribalet ◽  
P. M. Beigelman
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Two Phase ◽  
Sodium Permeability ◽  
Potential Spike ◽  
Presence And Absence

The present studies, designed to evaluate the contribution of Na+ to the mouse pancreatic beta-cell membrane potential, were performed utilizing intracellular microelectrodes. Complete removal of external sodium, in the presence of glucose, did not significantly affect spike peak potential. However, it caused a negative shift of the resting membrane potential, both in the presence and absence of glucose. After this initial hyperpolarization, the membrane gradually depolarized, the rate of depolarization being slower in the absence of glucose. This two-phase hyperpolarization-depolarization pattern remained when ouabain was added, both in the presence and absence of glucose. An increase of input resistance was associated with the slow depolarization. During this depolarization the maximum rate of rise (dV/dtmax) of the action potential (“spike”) decreased. There was no direct relationship between dV/dtmax and [Na]0. Readdition of low [Na]0 (14 mM) to a glucose medium reactivated the postburst hyperpolarization (PBH), even in the presence of ouabain. These observations indicate that there is a significant resting sodium permeability (PNa). However, the action potential (spike) is not generated by activation of a voltage-dependent (gated) sodium channel. The membrane depolarization after Na+ removal reflects concomitant inhibition of the Na+-K+ pump and decrease of potassium permeability (PK). The blockage of PBH in the absence of Na+ is not related to the inhibition of an oscillatory Na+-K+ pump but to the inactivation of a PK. Aside from its effect on the Na+-K+ pump, ouabain may stimulate PNa.

Microtubules modulate cardiomyocyte β-adrenergic response in cardiac hypertrophy

1998 ◽  
Vol 275 (5) ◽  
pp. H1707-H1716 ◽  
Author(s):  
Bradley M. Palmer ◽  
Scott Valent ◽  
Emma L. Holder ◽  
Howard D. Weinberger ◽  
Roger D. Bies
Keyword(s):  
Cardiac Hypertrophy ◽  
High Speed ◽  
Left Ventricular ◽  
Microtubule Assembly ◽  
Mechanical Relaxation ◽  
Sham Operation ◽  
Relaxation Dynamics ◽  
Sprague Dawley ◽  
Time To Peak ◽  
Adrenergic Response

The role of microtubules in modulating cardiomyocyte β-adrenergic response was investigated in rats with cardiac hypertrophy. Male Sprague-Dawley rats underwent stenosis of the abdominal aorta (hypertensive, HT) or sham operation (normotensive, NT). Echocardiography and isolated left ventricular cardiomyocyte dimensions demonstrated cardiac hypertrophy in the HT rats after 30 wk. Cardiomyocyte microtubule fraction was assayed by high-speed centrifugation and Western blot. In contrast to previous reports of increased microtubules after acute pressure overload, microtubule fraction for HT was significantly lower than that for NT. Cardiomyocytes were exposed to either 1 μM colchicine, 10 μM taxol, or equivalent volume of vehicle. Colchicine decreased microtubules, and taxol increased microtubules in both groups. Cardiomyocyte cytosolic calcium ([Ca2+]c) and shortening/relaxation dynamics were assessed during exposure to increasing isoproterenol concentrations. The β-adrenergic response for these variables in the HT group was blunted compared with NT. However, increased microtubule assembly by taxol partially recovered the normal β-adrenergic response for time to peak [Ca2+]c, time to peak shortening, and mechanical relaxation variables. Microtubule assembly may play a significant role in determining cardiomyocyte β-adrenergic response in chronic cardiac hypertrophy.

scholarly journals The Effect of Aconitine on the Giant Axon of the Squid

1964 ◽  
Vol 47 (4) ◽  
pp. 719-733 ◽  
Author(s):  
W. H. Herzog ◽  
R. M. Feibel ◽  
S. H. Bryant
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Giant Axon ◽  
Membrane Resistance ◽  
Repetitive Stimulation ◽  
Resting Membrane Potential ◽  
Sustained Activity ◽  
Frequency Of Stimulation ◽  
Sodium And Potassium

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.

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