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

Tanaka, Yasunori; Hisatome, Ichiro; Miyamoto, Jiro; Urashima, Tadashi; Ikeda, Kaoru; Yamanouchi, Yumi; Sasaki, Norihito; Kinugawa, Toru; Oginö, Kazuhíde; Igawa, Osamu; Yoshïda, Akio; Shigemasa, Chiaki; Kurata, Yasutaka; Satō, Ryōichi

doi:10.1016/s0005-2736(99)00043-7

Cited by 6 publications

(8 citation statements)

References 25 publications

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“…The enhancing effect of salicylate on quinidineinduced block of Na + channels does not depend on the tissue-specific structures of Na + channels In a previous study we found that salicylate selectively increased the quinidine-bound inactivated Na + channels, enhancing thereby both tonic block and UDB by quinidine in guinea-pig ventricular myocytes (23). The structural differences among channel proteins may account for tissue-specific sensitivity Fig.…”

Section: Discussionmentioning

confidence: 61%

“…As described previously (3,12), the voltagedependent inactivation curve of Na + channels (with quinidine) and concentration dependence of quinidine-induced tonic block were calculated for different K d values; the K dI value was determined for the state model to reproduce the experimental V h and IC 50 values, with the K dR value set equal to the experimental IC 50 at an HP of −140 mV. Rate constants for state transitions were formulated as functions of the Gibbs free energy composed of chemical and potential terms, as described in our previous articles (1,23).…”

Section: Methodsmentioning

confidence: 99%

“…4 Predicted voltage-dependent inactivation curve of the hH1 channel (with 6 μM quinidine) and concentration dependence of quinidine-induced tonic block (at HP = −100 mV) for the K dI value of 0.70 and 0.11 μM (K dR = 21.87 μM). Steadystate probability of a channel to be in the drug-free resting state (state R in Scheme 1) was calculated and normalized as described previously (23). The rate constants for the transition between the resting and inactivated states of hH1 channels are the same as used in Miake et al (16); the Gibbs free energy peak for the quinidine unbinding (dissociation from the channel) was assumed to be 34 (in RT unit).…”

Section: Effects Of Salicylate On Udb Of Human Namentioning

confidence: 99%

“…As for the effect of salicylate on cardiac myocytes, Tanaka et al (23) reported that it enhanced the action of Na + channel blockers with higher liposolubility by increasing their affinity for inactivated state channels. Since Na + channels in individual mutant Na + channel α subunit cDNAs, which were provided by Dr. Naomasa Makita.…”

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confidence: 99%

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Enhancing effects of salicylate on quinidine-induced block of human wild type and LQT3 related mutant cardiac Na+ channels

Urashima¹,

Kurata²,

Miake

et al. 2011

Biomed. Res.

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It is unknown whether salicylate enhances the action of antiarrhythmic agents on human Na + channels with state dependency and tissue specificity. We therefore investigated effects of salicylate on quinidine-induced block of human cardiac and skeletal muscle Na + channels. Human cardiac wild-type (hH1), LQT3-related mutant (ΔKPQ), and skeletal muscle (hSkM1) Na + channel α subunits were expressed in COS7 cells. Effects of salicylate on quinidine-induced tonic and usedependent block of Na + channel currents were examined by the whole-cell patch-clamp technique. Salicylate enhanced the quinidine-induced tonic and use-dependent block of both hH1 and hSkM1 currents at a holding potential (HP) of −100 mV but not at −140 mV. Salicylate decreased the IC 50 value for the quinidine-induced tonic block of hH1 at an HP of −100 mV, and produced a negative shift in the steady-state inactivation curve of hH1 in the presence of quinidine. According to the modulated receptor theory, it is probable that salicylate decreases the dissociation constant for quinidine binding to inactivated-state channels. Furthermore, salicylate significantly enhanced the quinidine-induced tonic and use-dependent block of the peak and steady-state ΔKPQ channel currents. The results suggest that salicylate enhances quinidine-induced block of Na + channels via increasing the affinity of quinidine to inactivated state channels.Acetylsalicylic acid, the most widely studied antiplatelet drug, suppresses platelet aggregation by inhibiting cyclo-oxygenase. Salicylic acid (C 6 H 4 (OH)COOH) belongs to the group of aromatic monocarboxylic acids, which by themselves do not have an anesthetic action. However, monocarboxylic acids such as salicylic, benzoic, acetic, propionic and butyric acid have been reported to enhance the action of local anesthetics (7, 13). In particular, monocarboxylic acids containing a lipophilic moiety such as an aliphatic hydrocarbon chain or aromatic ring can enhance the action of local anesthetics in nerves; indeed, salicylate has been reported to enhance the blocking action of procainamide on sodium (Na + ) channels in nerves (7). And Katsuki et al. (13) demonstrated that salicylate decreased the intracellular pH, which resulted in an increase of the proportion of charged molecules of procaine and the enhancement of its local anesthetic action on nerves.As for the effect of salicylate on cardiac myocytes, Tanaka et al. (23) reported that it enhanced the action of Na + channel blockers with higher liposolubility by increasing their affinity for inactivated state channels. Since Na + channels in individual

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Section: Discussionmentioning

confidence: 61%

Section: Methodsmentioning

confidence: 99%

Section: Effects Of Salicylate On Udb Of Human Namentioning

confidence: 99%

mentioning

confidence: 99%

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Enhancing effects of salicylate on quinidine-induced block of human wild type and LQT3 related mutant cardiac Na+ channels

Urashima¹,

Kurata²,

Miake

et al. 2011

Biomed. Res.

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“…Atrial myocytes were enzymatically isolated as described previously (17). Cells were dispersed in the recording bath and superfused with Tyrode's solution containing (in mmol/l) 140 NaCl, 5.4 KCl, 0.5 MgCl2, 1.8 CaCl2, 5 HEPES and 5.5 glucose (pH 7.4).…”

Section: Cell Isolationmentioning

confidence: 99%

Inhibition of Inward Rectifier K+ Currents by Angiotensin II in Rat Atrial Myocytes: Lack of Effects in Cells from Spontaneously Hypertensive Rats

et al. 2006

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Analysis of moricizine block of sodium current in isolated guinea-pig atrial myocytes

Ahmmed

Hisatome

Kurata

et al. 2002

Vascular Pharmacology

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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

Cited by 6 publications

References 25 publications

Enhancing effects of salicylate on quinidine-induced block of human wild type and LQT3 related mutant cardiac Na+ channels

Enhancing effects of salicylate on quinidine-induced block of human wild type and LQT3 related mutant cardiac Na+ channels

Inhibition of Inward Rectifier K+ Currents by Angiotensin II in Rat Atrial Myocytes: Lack of Effects in Cells from Spontaneously Hypertensive Rats

Analysis of moricizine block of sodium current in isolated guinea-pig atrial myocytes

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