scholarly journals Effects of long-term amiodarone on action potential and ionic currents in rabbit ventricular myocytes.

1993 ◽  
Vol 61 ◽  
pp. 269
Author(s):  
Kaichiro Kamiya ◽  
Jianhua Cheng ◽  
Ryoko Suzuki ◽  
Hirokazu Iwata ◽  
Itsuo Kodama ◽  
...  
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Ionic Currents ◽  
Rabbit Ventricular Myocytes

Basis for tetrodotoxin and lidocaine effects on action potentials in dog ventricular myocytes

1988 ◽  
Vol 254 (6) ◽  
pp. H1157-H1166 ◽  
Author(s):  
J. A. Wasserstrom ◽  
J. J. Salata
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Ionic Currents ◽  
Detectable Effect ◽  
Na Channel ◽  
Na Current ◽  
Voltage Range ◽  
Purkinje Fibers ◽  
Ventricular Cells

We studied the effects of tetrodotoxin (TTX) and lidocaine on transmembrane action potentials and ionic currents in dog isolated ventricular myocytes. TTX (0.1-1 x 10(-5) M) and lidocaine (0.5-2 x 10(-5) M) decreased action potential duration, but only TTX decreased the maximum rate of depolarization (Vmax). Both TTX (1-2 x 10(-5) M) and lidocaine (2-5 x 10(-5) M) blocked a slowly inactivating toward current in the plateau voltage range. The voltage- and time-dependent characteristics of this current are virtually identical to those described in Purkinje fibers for the slowly inactivating inward Na+ current. In addition, TTX abolished the outward shift in net current at plateau potentials caused by lidocaine alone. Lidocaine had no detectable effect on the slow inward Ca2+ current and the inward K+ current rectifier, Ia. Our results indicate that 1) there is a slowly inactivating inward Na+ current in ventricular cells similar in time, voltage, and TTX sensitivity to that described in Purkinje fibers; 2) both TTX and lidocaine shorten ventricular action potentials by reducing this slowly inactivating Na+ current; 3) lidocaine has no additional actions on other ionic currents that contribute to its ability to abbreviate ventricular action potentials; and 4) although both agents shorten the action potential by the same mechanism, only TTX reduces Vmax. This last point suggests that TTX produces tonic block of Na+ current, whereas lidocaine may produce state-dependent Na+ channel block, namely, blockade of Na+ current only after Na+ channels have already been opened (inactivated-state block).

Electrophysiological and functional effects of adenosine on ventricular myocytes of various mammalian species

1996 ◽  
Vol 271 (4) ◽  
pp. C1233-C1243 ◽  
Author(s):  
Y. Song ◽  
L. Belardinelli
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Mammalian Species ◽  
Outward Current ◽  
Binding Studies ◽  
Outward Currents ◽  
K Current ◽  
Rabbit Ventricular Myocytes ◽  
A1 Adenosine Receptors

The goal of this study was to determine the electrophysiological and functional effects of adenosine on ventricular myocytes of guinea pig, rabbit, rat, and ferret hearts. Adenosine (100 microM) shortened the action potential durations of rat and ferret myocytes by 14 +/- 1 and 57 +/- 7%, reduced the amplitudes of cell twitch shortening by 13 +/- 1 and 54 +/- 5%, and increased outward currents by 15 +/- 4 and 55 +/- 5%, respectively, but had no effect on guinea pig and rabbit myocytes. The properties of adenosine-activated outward current in rat and ferret ventricular myocytes indicated that this current is the adenosine-sensitive K+ current [IK(Ado)]. Adenosine had no significant effect on basal Ca2+ current but specifically inhibited isoproterenol-stimulated L-type Ca2+ current in myocytes of all species studied. Binding studies revealed that the density of A1 adenosine receptors (A1AdoR) was highest in ferret and lowest in rabbit myocytes, but the differential effects of adenosine among species could not be solely explained by differences in A1AdoR density. In summary, adenosine shortened the action potential and reduced the twitch shortening of rat and ferret but not of guinea pig and rabbit ventricular myocytes. Shortening of the action potential was associated with the activation of IK(Ado). The anti-beta-adrenergic action of adenosine appeared to be independent of species.

Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. H1270-H1277 ◽  
Author(s):  
Gui-Rong Li ◽  
Min Zhang ◽  
Leslie S. Satin ◽  
Clive M. Baumgarten
Keyword(s):  
Action Potential ◽  
Cell Volume ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Current Clamp ◽  
Osmotic Swelling ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Fura 2 ◽  
Rabbit Ventricular Myocytes

We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current ( I Ca-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given I Ca-L, and later, both I Ca-L and the Ca2+ transient are inhibited.

Depression of excitability by sphingosine 1-phosphate in rat ventricular myocytes

1998 ◽  
Vol 275 (6) ◽  
pp. H2291-H2299 ◽  
Author(s):  
Karen L. MacDonell ◽  
David L. Severson ◽  
Wayne R. Giles
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Sodium Current ◽  
Potassium Conductance ◽  
Ionic Currents ◽  
Stimulus Current ◽  
Muscle Action Potential ◽  
Action Potential Waveform ◽  
Sphingosine 1 Phosphate ◽  
Electrophysiological Effects

Sphingosine 1-phosphate (S-1- P) is a bioactive sphingolipid that is released from activated platelets. Extracellular S-1- P augments an inwardly rectifying potassium conductance in cultured atrial preparations, but the electrophysiological effects of this compound in the ventricle are unknown. The electrophysiological effects of S-1- P were examined in single myocytes from rat ventricular muscle. Action potential waveforms and underlying ionic currents in the presence and absence of 3 μM S-1- P (1–6 min) were recorded. S-1- P increased the minimum stimulus current needed to elicit an action potential by ∼100 pA. Pertussis toxin or preexposure to S-1- P did not alter this effect. The action potential waveform was unchanged by S-1- P. The inward sodium current ( I Na) was examined in a range of membrane potentials just negative to the potential for firing an action potential. S-1- P reversibly inhibited peak I Na by ∼50 pA, whereas the inward rectifier potassium current was not significantly changed. The results of this study suggest that S-1- P inhibits rat ventricular excitability by reducing I Na.

In Vitro  Electrophysiologic Effects of Morphine in Rabbit Ventricular Myocytes

2005 ◽  
Vol 103 (2) ◽  
pp. 280-286 ◽  
Author(s):  
Guo-Sheng Xiao ◽  
Jing-Jun Zhou ◽  
Guan-Ying Wang ◽  
Chun-Mei Cao ◽  
Gui-Rong Li ◽  
...  
Keyword(s):  
Action Potential ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Ventricular Myocytes ◽  
Cardiac Action Potential ◽  
Resting Membrane Potential ◽  
Opioid Receptor Antagonist ◽  
Cardiac Action ◽  
K Current ◽  
Rabbit Ventricular Myocytes

Background Morphine is widely used in patients undergoing surgical operations and is also reported to mediate cardioprotection of preconditioning. The current study determined effects of morphine at therapeutic to pharmacologic concentrations on cardiac action potential, L-type Ca2+ current (ICa.L), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1) in isolated rabbit ventricular myocytes. Methods Ventricular myocytes were enzymatically isolated from rabbit hearts. Action potential and membrane currents were recorded in current and voltage clamp modes. Results Morphine at concentrations from 0.01 to 1 microM significantly prolonged cardiac action potential, and at 0.1 and 1 microM slightly but significantly hyperpolarized the resting membrane potential. In addition, morphine at 0.1 microM significantly augmented ICa.L (at +10 mV) from 5.9 +/- 1.9 to 7.3 +/- 1.7 pA/pF (by 23%; P < 0.05 vs. control) and increased IK1 (at -60 mV) from 2.8 +/- 1.0 to 3.5 +/- 0.9 pA/pF (by 27%; P < 0.05 vs. control). Five microM naltrindole (a selective delta-opioid receptor antagonist) or 5 microM norbinaltorphimine (a selective kappa-opioid receptor antagonist) prevented the increase in ICa.L induced by morphine, but 5 microM CTOP (a selective mu-opioid receptor antagonist) did not. The three types of opioid antagonists did not affect the augmentation of IK1 by morphine. Morphine had no effect on IK. Conclusions These results indicate that morphine prolongs action potential duration by increasing ICa.L, an effect mediated by delta- and kappa-opioid receptors. It also hyperpolarizes cardiac resting membrane potential by increasing IK1, which is not mediated by opioid receptors.

Sign in / Sign up

Export Citation Format

Share Document