title: Effect of chronic exercise and Angiotensin-converting enzyme inhibition on rodent thoracic aorta.
abstract: Vascular reactivity can be modulated by local physical factors as well as pharmacologic manipulations. The aim of this study was to evaluate the effects of chronic exercise (EX) with or without the ACEI captopril (CAP) on vascular reactivity. Sixty-four Sprague-Dawley male rats were randomized into 4 groups (n = 16): group 1, control; group 2, captopril; group 3, exercise; and group 4, exercise and captopril. After 10 weeks of treatment, rats were killed, and their thoracic aortas harvested. Vascular reactivity was studied in an organ chamber (n = 12). Aortic endothelium constitutive nitric oxyde synthase (NOS3) expression was determined by Western blot analysis (n = 4). Endothelial-dependent relaxation was increased in both CAP and EX rats relative to the control group. Maximal aortic relaxations were enhanced in the CAP group, and potencies of these mediators were enhanced in the EX group (P < 0.05 versus control). Combined treatment did not result in a synergistic effect. NOS3 relative expressions were: group 1, 100%; group 2, 241%; group 3, 64%; and group 4, 108%. Exercise enhanced both potencies and efficacies of the mediators studied, whereas CAP increased mainly their efficacies. NOS3 protein expression was up-regulated in CAP-treated rats but not in exercised rats. These findings suggest different mechanisms for the observed increased vascular reactivity.
authors.affiliation: Department of Surgery, Montreal Heart Institute, Montreal, Quebec, Canada.
authors.forename: Stéphane
authors.initials: S
authors.lastname: Elkouri
authors.forename: Philippe
authors.initials: P
authors.lastname: Demers
authors.forename: Martin G
authors.initials: MG
authors.lastname: Sirois
authors.forename: André
authors.initials: A
authors.lastname: Couturier
authors.forename: Raymond
authors.initials: R
authors.lastname: Cartier
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000284:Administration, Oral; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000493:pharmacokinetics*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D001794:Blood Pressure / Q000502:physiology; D015153:Blotting, Western / Q000379:methods; D001835:Body Weight / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002216:Captopril / Q000008:administration & dosage / Q000493:pharmacokinetics; D015536:Down-Regulation / Q000502:physiology; D004334:Drug Administration Schedule; D004353:Drug Evaluation, Preclinical / Q000379:methods; D004730:Endothelium, Vascular / Q000737:chemistry / Q000187:drug effects / Q000648:ultrastructure; D006321:Heart; D006632:Histamine / Q000494:pharmacology; D007120:Immunochemistry / Q000379:methods; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D009929:Organ Size / Q000502:physiology; D010656:Phenylephrine / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000379:methods* / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D015854:Up-Regulation; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014841:von Willebrand Factor / Q000737:chemistry / Q000276:immunology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007476:Ionophores; D014841:von Willebrand Factor; D010656:Phenylephrine; D000244:Adenosine Diphosphate; D006632:Histamine; D002216:Captopril; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D000109:Acetylcholine; D002118:Calcium