scholarly journals Enhancing effects of salicylate on tonic and phasic block of Na+ channels by class 1 antiarrhythmic agents in the ventricular myocytes and the guinea pig papillary muscle

1999 ◽  
Vol 1418 (2) ◽  
pp. 320-334 ◽  
Author(s):  
Yasunori Tanaka ◽  
Ichiro Hisatome ◽  
Jiro Miyamoto ◽  
Tadashi Urashima ◽  
Kaoru Ikeda ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Papillary Muscle ◽  
Ventricular Myocytes ◽  
Antiarrhythmic Agents ◽  
Na Channels ◽  
Phasic Block ◽  
Class 1 ◽  
Block Of Na Channels

Properties of veratridine-modified single Na+ channels in guinea pig ventricular myocytes

1992 ◽  
Vol 24 ◽  
pp. 273
Author(s):  
Akihiko Sunami ◽  
Tetsuo Sasano ◽  
Ayako Matsunaga ◽  
Zheng Fan ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Na Channels

Electrophysiological safety of sibutramine HCl

2008 ◽  
Vol 27 (7) ◽  
pp. 553-558 ◽  
Author(s):  
KS Kim ◽  
SJ Park ◽  
HA Lee ◽  
DK Kim ◽  
EJ Kim
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Papillary Muscle ◽  
Ventricular Myocytes ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cardiovascular Side Effects ◽  
Blocking Effects ◽  
Inward Currents ◽  
Sibutramine Hcl

Sibutramine is known to induce cardiovascular side effects such as tachycardia, vasodilation, and hypertension. The present study was aimed to examine the effects of sibutramine on action potential of guinea pig papillary muscle, recombinant hERG currents (IhERG), and inward currents (INa and ICa) of rat ventricular myocytes. Sibutramine at 30 μg/mL induced a shortening of action potential duration (APD) of guinea pig papillary muscle; on average, APD30 and APD90 were shortened by 23% and 17% at a stimulation rate of 1 Hz, respectively. Sibutramine suppressed the following currents: IhERG (IC50:2.408 ± 0.5117 μg/mL), L-type Ca current (IC50:2.709 ± 0.4701 μg/mL), and Na current (IC50:7.718 ± 1.7368 μg/mL). Sibutramine blocked IhERG, ICa, and INa in a concentration-dependent manner. In conclusion, sibutramine exerted a shortening effect on APD in guinea pig papillary muscle through its more powerful blocking effects on ICa and INa rather than IhERG.

scholarly journals Inhibition of Na+ channels by Cl transport blocker DIDS in guinea pig ventricular myocytes.

1996 ◽  
Vol 71 ◽  
pp. 310
Author(s):  
Jie Liu ◽  
Zhong-Fang Lai ◽  
Naofurai Tokutorai ◽  
Katsuhide Nishi
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Na Channels ◽  
Cl Transport

Properties of veratridine-modified single Na+ channels in guinea pig ventricular myocytes

1993 ◽  
Vol 264 (2) ◽  
pp. H454-H463 ◽  
Author(s):  
A. Sunami ◽  
T. Sasano ◽  
A. Matsunaga ◽  
Z. Fan ◽  
T. Swanobori ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Voltage Dependence ◽  
Single Channel ◽  
Ventricular Myocytes ◽  
Simultaneous Occurrence ◽  
Na Channels ◽  
Patch Clamp Technique ◽  
Open Time ◽  
High Event ◽  
Event Times

Modification of single Na+ channels by the alkaloid neurotoxin veratridine was investigated in guinea pig ventricular myocytes using the cell-attached configuration of the patch-clamp technique. Pipette application of veratridine (50 microM) induced long-lasting openings with two different single-channel conductances of 7.6 and 3.0 pS, in addition to normal type of short openings with a single-channel conductance of 16 pS. The veratridine-modified high- and low-conductance channels appeared commonly, and they could coexist with the normal one in the same patch. The open-time distributions for the high- and low-conductance channels could be fitted by a single exponential. The mean open time for the high- and low-conductance events ranged between 19.1 ms at -120 mV and 86.0 ms at -10 mV and between 4.5 ms at -120 mV and 16.2 ms at -10 mV, respectively. The closed-time distributions for the two conductance channels consisted of at least two components, and their values and voltage dependence were similar. External Ca2+ block resulted in an apparent reduction of unitary current amplitudes with a similar voltage dependence and affinity for Ca2+ in the high- and low-conductance channels. However, the low-conductance channel was more resistant to tetrodotoxin than the high one. The probability of simultaneous occurrence of the high and low events was equal to the product of the probabilities of occurrence of the high event times that of the low event. Furthermore, we observed modified channel openings after a normal opening for the two conductance channels and a modified one turning into a normal one for the high-conductance channel. It is concluded that veratridine induces the two different types of modified Na+ channels in cardiac myocytes and these are correlated with normal openings.

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