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Tonic block of the Na + current in single atrial and ventricular guineapig myocytes, by a new antiarrhythmic drug, Ro 22‐9194
Author(s) -
Hiroe K.,
Hisatome I.,
Tanaka Y.,
Ahmmed GU,
Sasaki N.,
Shimoyama M.,
Tsuboi M.,
Inoue Y.,
Manabe I.,
Yamamoto Y.,
Ohtahata A.,
Kinugawa T.,
Ogino K.,
Igawa O.,
Yoshida A.,
Shigemasa C.,
Sato R.
Publication year - 1997
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1997.tb00202.x
Subject(s) - myocyte , atrial myocytes , medicine , atrium (architecture) , tonic (physiology) , chemistry , patch clamp , cardiology , electrophysiology , endocrinology , atrial fibrillation
Summary— Ro 22‐9194 reduced the Na + current in the atrial myocytes as well as ventricular myocytes in a tonic block fashion. Ro 22‐9194 had a higher affinity to the inactivated state Na + channels (Kd 1 = 3.3 μM in atrial myocytes, Kd 1 = 10.3 μM in ventricular myocytes) than to those in the rested state (Kd R = 91 μM in atrial myocytes, Kd R = 180 μM in ventricular myocytes), which indicated that Ro 22‐9194 had a higher affinity to the Na + channels in atrial myocytes than in ventricular myocytes. Ro 22‐9194 shifted the inactivation curve in the hyperpolarized direction in both atrial and ventricular myocytes. These findings suggest that Ro 22‐9194 more strongly inhibited the Na + channel of the atrial myocytes of the diseased hearts with the depolarized membranes potentials than the Na + channels in ventricular myocytes.