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Cardiac electrophysiological actions of captopril: lack of direct antiarrhythmic effects
Author(s) -
Hemsworth Paul D.,
Pallandi Regan T.,
Campbell Terence J.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb16881.x
Subject(s) - captopril , electrophysiology , depolarization , cardiology , medicine , membrane potential , stimulation , chemistry , anesthesia , blood pressure , biochemistry
1 Standard microelectrode techniques were used to study the effects of captopril (1, 10 and 100 μ m ) on action potentials recorded from guinea‐pig ventricular cells and sinoatrial node cells. 2 Captopril had no effect on the maximum rate of depolarization () of ventricular action potentials in cells exposed to either normal Locke solution or ‘simulated ischaemic’ solution (K + = 11.2 mM; pH = 6.4; P o 2 < 80 mmHg), nor was there any augmentation of the normal small decline in with increasing stimulation rate (range of interstimulus intervals = 2400 ms to 300 ms). 3 Captopril had no effect on the duration of ventricular action potentials, nor did it alter the shortening seen on exposure to simulated ischaemia. 4 Captopril did not alter spontaneous sinus cycle length or any recorded parameter of sinus node action potentials. 5 It is concluded that any antiarrhythmic effects observed during clinical use of captopril are most unlikely to be due to direct actions of the drug on cardiac cell membrane properties.