title: Angiotensin converting enzyme inhibition reduces cardiovascular responses to acute stress in myocardially infarcted and chronically stressed rats.
abstract: Previous studies showed that chronically stressed and myocardially infarcted rats respond with exaggerated cardiovascular responses to acute stress. The present experiments were designed to elucidate whether this effect can be abolished by treatment with the angiotensin converting enzyme (ACE) inhibitor captopril. Sprague Dawley rats were subjected either to sham surgery (Groups 1 and 2) or to myocardial infarction (Groups 3 and 4). The rats of Groups 2 and 4 were also exposed to mild chronic stressing. Four weeks after the operation, mean arterial blood pressure (MABP) and heart rate (HR) were measured under resting conditions and after application of acute stress. The cardiovascular responses to the acute stress were determined again 24 h after administration of captopril orally. Captopril significantly reduced resting MABP in each group. Before administration of captopril, the maximum increases in MABP evoked by the acute stressor in all (infarcted and sham-operated) chronically stressed rats and also in the infarcted nonchronically stressed rats were significantly greater than in the sham-operated rats not exposed to chronic stressing. These differences were abolished by captopril. The results suggest that ACE may improve tolerance of acute stress in heart failure and during chronic stressing.
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Cudnoch-Jedrzejewska
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: K
authors.initials: K
authors.lastname: Czarzasta
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: L
authors.initials: L
authors.lastname: Puchalska
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Dobruch
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: O
authors.initials: O
authors.lastname: Borowik
authors.affiliation: Department of Internal Medicine and Endocrinology, Medical University of Warsaw, Ulica Banacha 1a, 02-097 Warsaw, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Pachucki
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Ulica Pawinskiego 3c, 02-106 Warsaw, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Szczepanska-Sadowska
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage*; D000818:Animals; D002319:Cardiovascular System / Q000187:drug effects; D006333:Heart Failure / Q000188:drug therapy* / Q000473:pathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology; D007703:Peptidyl-Dipeptidase A; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007703:Peptidyl-Dipeptidase A