title: Angiotensin converting enzyme inhibition prevents trophic and hypertensive effects of an antagonist of adenosine receptors.
abstract: The continuous infusion of 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), a non-selective antagonist of adenosine receptors, causes hypertension and marked cardiovascular structural changes in Wistar rats. Adenosine inhibits noradrenaline and renin release. We investigated the effects of sympathetic denervation, evaluated renin activity and the influence of angiotensin converting enzyme inhibition in DPSPX-treated rats. Captopril was given (30 or 100 mg kg(-l) day(-l); p.o.) from day -l to day 28. On day 0, constant infusions of DPSPX (90 microg kg(-l) h(-l); i.p.) or vehicle were started. On day 28, fragments of the left ventricle, mesenteric and tail arteries were processed for morphological studies. Plasma renin activity was increased in DPSPX-treated animals. Sympathetic denervation delayed and partially prevented blood pressure rise. Angiotensin converting enzyme inhibition prevented DPSPX-induced hypertension and morphological changes. Our results, although pointing to the involvement of the sympathetic system, suggest that other mechanisms are involved. We could not differentiate between the trophic and anti-hypertensive effects of angiotensin converting enzyme inhibition.
authors: Institute of Pharmacology and Therapeutics, Faculty of Medicine of Porto and IBMC, University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal.
authors: Teresa
authors: T
authors: Sousa
authors: Manuela
authors: M
authors: Morato
authors: António
authors: A
authors: Albino-Teixeira
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D048429:Cell Size / Q000187:drug effects; D006321:Heart / Q000254:growth & development; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D006984:Hypertrophy / Q000139:chemically induced / Q000517:prevention & control; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects; D009929:Organ Size / Q000187:drug effects; D016627:Oxidopamine / Q000494:pharmacology; D007703:Peptidyl-Dipeptidase A / Q000187:drug effects*; D058915:Purinergic P1 Receptor Antagonists; D051381:Rats; D017208:Rats, Wistar; D013562:Sympathectomy; D013565:Sympatholytics / Q000494:pharmacology; D013623:Tail / Q000098:blood supply; D014970:Xanthines / Q000494:pharmacology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D058915:Purinergic P1 Receptor Antagonists; D013565:Sympatholytics; D014970:Xanthines; C053896:1,3-dipropyl-8-(4-sulfophenyl)xanthine; D016627:Oxidopamine; D002216:Captopril; D007703:Peptidyl-Dipeptidase A