Cardiac Antiarrhythmic Agents

Participation of α1 adrenoceptors in the proarrhythmic effect of class III antiarrhythmic agents in halothane anesthetized dogs

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)49324-4 ◽

1992 ◽

Vol 58 ◽

pp. 277

Author(s):

Hiroyuki Suga ◽

Takashi Satoh ◽

Masaaki Ishii ◽

Tatsuro Yokoyama ◽

Joji Kamiya

Keyword(s):

Antiarrhythmic Agents ◽

Class Iii ◽

Proarrhythmic Effect ◽

Anesthetized Dogs

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Study of antiarrhythmic agents on cardiovascular and CNS actions in experimentally-induced arrhythmia rats, (report II).

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)39219-4 ◽

1991 ◽

Vol 55 ◽

pp. 277

Author(s):

Masaaki Hayashi ◽

Hiromi Matsuda ◽

Katsuhiko Sato ◽

Ichie Hara ◽

Jian-wei Li ◽

...

Keyword(s):

Antiarrhythmic Agents ◽

Experimentally Induced

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Antiarrhythmic agents inhibit the formation of thromboxane (TX) in platelets from spontaneously hyperten ive rats (SHR)

Prostaglandins Leukotrienes and Medicine ◽

10.1016/0262-1746(87)90105-3 ◽

1987 ◽

Vol 26 (2) ◽

pp. 105-113 ◽

Cited By ~ 2

Author(s):

Judy Lucas ◽

Peter S. Chan ◽

Peter Cervoni

Keyword(s):

Antiarrhythmic Agents

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Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents.

The Journal of General Physiology ◽

10.1085/jgp.96.1.195 ◽

1990 ◽

Vol 96 (1) ◽

pp. 195-215 ◽

Cited By ~ 1050

Author(s):

M C Sanguinetti ◽

N K Jurkiewicz

Keyword(s):

Antiarrhythmic Agent ◽

Reversal Potential ◽

Differential Sensitivity ◽

Inward Rectification ◽

Delayed Rectifier ◽

Antiarrhythmic Agents ◽

Class Iii ◽

Activation Curve ◽

Voltage Range ◽

K Current

An envelope of tails test was used to show that the delayed rectifier K+ current (IK) of guinea pig ventricular myocytes results from the activation of two outward K+ currents. One current was specifically blocked by the benzenesulfonamide antiarrhythmic agent, E-4031 (IC50 = 397 nM). The drug-sensitive current, "IKr" exhibits prominent rectification and activates very rapidly relative to the slowly activating drug-insensitive current, "IKs." IKs was characterized by a delayed onset of activation that occurs over a voltage range typical of the classically described cardiac IK. Fully activated IKs, measured as tail current after 7.5-s test pulses, was 11.4 times larger than the fully activated IKr. IKr was also blocked by d-sotalol (100 microM), a less potent benzenesulfonamide Class III antiarrhythmic agent. The activation curve of IKr had a steep slope (+7.5 mV) and a negative half-point (-21.5 mV) relative to the activation curve of IKs (slope = +12.7 mV, half-point = +15.7 mV). The reversal potential (Erev) of IKr (-93 mV) was similar to EK (-94 mV for [K+]o = 4 mM), whereas Erev of IKs was -77 mV. The time constants for activation and deactivation of IKr made up a bell-shaped function of membrane potential, peaking between -30 and -40 mV (170 ms). The slope conductance of the linear portion of the fully activated IKr-V relation was 22.5 S/F. Inward rectification of this relation occurred at potentials greater than -50 mV, resulting in a voltage-dependent decrease in peak IKr at test potentials greater than 0 mV. Peak IKr at 0 mV averaged 0.8 pA/pF (n = 21). Although the magnitude of IKr was small relative to fully activated IKs, the two currents were of similar magnitude when measured during a relatively short pulse protocol (225 ms) at membrane potentials (-20 to +20 mV) typical of the plateau phase of cardiac action potentials.

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