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EFFECTS OF ERVATAMINE CHLORHYDRATE ON CARDIAC MEMBRANE CURRENTS IN FROG ATRIAL FIBRES
Author(s) -
SAUVIAT MARTINPIERRE
Publication year - 1980
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.1476-5381.1980.tb10907.x
Subject(s) - chemistry , membrane potential , sucrose gap , biophysics , alkaloid , electrophysiology , tetrodotoxin , dissociation constant , sodium , voltage clamp , stereochemistry , biochemistry , medicine , biology , receptor , organic chemistry
1 The effects of a new alkaloid, ervatamine, on transmembrane currents of frog atrial fibres were studied by the double sucrose gap voltage clamp technique. 2 Ervatamine (2.8 × 10 −4 m ) blocked the action potential without altering the resting membrane potential. 3 The alkaloid depressed the peak I Na . The dissociation constant for the blocking effect of ervatamine on g Na fast was 2.35 × 10 −5 m with a one to one relationship between the drug molecule and the Na channel. Ervatamine did not alter the apparent equilibrium potential for Na, as well as the activation and inactivation parameters of g Na fast . This suggests that the alkaloid inhibitory effect on g Na can be attributed to a reduction in . 4 Ervatamine prolonged the rate of reactivation of the Na system. It inhibited g Na in a frequencydependent manner; this indicates that the alkaloid acts on open Na channels i.e. that the drug has to enter the channel or cross the membrane to produce the block. 5 Ervatamine inhibited I Na slow which occurs in Ca‐free, tetrodotoxin‐containing solutions and moderately decreased I ca which occurs in Na‐free solutions. The drug increased the background K current (I K1 ) and did not alter the time‐dependent K current (I x1 ). 6 The present study shows that ervatamine is a good inhibitor of both fast and slow g Na . This drug also shares some common electrophysiological properties with antiarrhythmic drugs namely: the frequency‐dependent inhibition of the fast g Na and the ability to slow the reactivation of the Na carrying system.