Summary
Cholinergic agents exert no direct effect on the fast Na+ inward current but may influence the binding characteristic of class I antiarrhythmic drugs in atrial myocardium by shortening the action potential (AP) duration or by increasing the resting potential (RP). In order to examine such possible interactions we performed experiments using conventional intracellular microelectrodes on isolated preparations of rabbit atrial myocardium (Ke 2.7 mM, temperature 32°C). At first the influence of the cholinergic agent carbachol (1 mg/l=6.7×10−6 M) on the RP and AP was examined at different stimulation rates (1.0, 2.5, and 3.3 Hz). Thereafter measurements were repeated under the influence of lidocaine (10 mg/l=2.2×10−5 M) or quinidine (5 mg/l=2.2×10−5M) alone and in combination with carbachol (1 mg/l).
Similar content being viewed by others
References
Bean BP, Cohen CJ, Tsien RW (1982) Block of cardiac sodium channels by tetrodotoxin and lidocaine. Sodium current and Vmax experiments. In: Paes de Carvalho A, Hoffman BF, Lieberman M (eds). Normal and abnormal conduction in the heart. Futura publishing company, Mount Kisco, New York, 189–206
Chen CM, Gettes LS, Katzung BG (1975) Effect of lidocaine and quinidine on steady-state characteristics and recovery kinetics of (dv/dt)max in guinea pig ventricular myocardium. Circ Res 37:20–29
Clarkson CW, Hondeghem LM (1985) Evidence for a specific receptor site for lidocaine, quinidine and bupivacaine associated with cardiac sodium channels in guinea pig ventricular myocardium. Circ Res 56:496–506
Gettes LS, Reuter H (1974) Slow recovery from inactivation of inward currents in mammalian myocardial fibers. J Physiol 240:703–724
Giles WR, Noble SJ (1976) Changes in membrane currents in bullfrog atrium produced by acetyl choline. J Physiol 261:103–123
Hille B (1977) Local anesthetics: Hydrophilic and hydrophobic pathways to the drug receptor reaction. J Gen Physiol 69:497–515
Hondeghem LM (1978) Validity of Vmax as a measure of the sodium current in cardiac and nervous tissues. Biophys J 23:147–152
Hondeghem LM, Katzung BG (1980) Test of a model of antiarrhymic drug action. Circ Res 61:1217–1224
Hondeghem LM, Katzung BG (1984) Antiarrhythmic agents: The modulated receptor mechanism of action of sodium and calcium channel-blocking drugs. Ann Rev Pharmacol Toxicol 24:387–423
Hutter OF (1961) Ion movements during vagus inhibition of the heart. In: Florey (ed) Nervous inhibition. Pergamon Press, Oxford pp 114–123
Mirro MJ, Watanabe AM, Bailey JC (1980) Electrophysiological effects of disopyramide and quinidine on guinea pig atria and canine cardiac Purkinje fibers. Dependence of the underlying cholinergic tone. Circ Res 46:660–668
Strichartz GR, Cohen I (1978) Vmax as a measure of Gna in nerve and cardiac membranes. Biophys J 23:153–156
Weidmann S (1955) The effect of the cardiac membrane potential on the rapid availability of the sodium-carrying system. J Physiol 127:213–224
Author information
Authors and Affiliations
Additional information
Supported by the Deutsche Forschungsgemeinschaft (La 471/2-1)
Rights and permissions
About this article
Cite this article
Langenfeld, H., Köhler, C., Haverkampf, K. et al. Electrophysiological interactions between carbachol and class I antiarrhythmic drugs (lidocaine, quinidine)—experimental studies in rabbit atrial myocardium. Basic Res Cardiol 84, 55–62 (1989). https://doi.org/10.1007/BF01907003
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF01907003