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Effects of lisinopril on electromechanical properties and membrane currents in guinea‐pig cardiac preparations
Author(s) -
Valenzuela Carmen,
Pérez Onésima,
Casis Oscar,
Duarte Juan,
PérezVizcaino Francisco,
Delpón Eva,
Tamargo Juan
Publication year - 1993
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.1476-5381.1993.tb13656.x
Subject(s) - lisinopril , isoprenaline , contraction (grammar) , medicine , inotrope , electrophysiology , chemistry , endocrinology , guinea pig , stimulation , angiotensin converting enzyme , blood pressure
1 The effects of the angiotensin‐converting enzyme inhibitor, lisinopril, were studied in guinea‐pig atria and papillary muscles and in single isolated ventricular cells. 2 In isolated right atria, lisinopril (0.001–10 μ m ) decreased the amplitude and rate of the spontaneous contractions. In electrically driven left atria this negative inotropic effect was accompanied by a shortening of the time to peak tension and time for total contraction. 3 Lisinopril did not modify the electrophysiological characteristics of the ventricular action potentials recorded in papillary muscles perfused with normal Tyrode solution or elicited by isoprenaline in papillary muscles perfused with 27 m m K Tyrode solution. 4 In single ventricular cells, lisinopril (10 μ m ) had no effect on the inward L‐type Ca 2+ ( I Ca,L ), the inward rectifier ( I K1 ) or the delayed rectifier K + currents ( I K ). However, it abolished the stimulation‐dependent facilitation of the L‐type Ca 2+ current. 6 These results indicate that the negative inotropic effect of lisinopril cannot be explained by a decrease in Ca 2+ entry through L‐type channels and suggest that lisinopril may possibly act at an intracellular site to reduce contractile force.