title: Arterial effects of angiotensin converting enzyme inhibition in renovascular and spontaneously hypertensive rats.
abstract: The effects of chronic therapy, using an angiotensin converting enzyme (ACE) inhibitor (S9490-3 perindopril, 1 mg/kg), on the mechanical and structural properties of large arteries were studied in two-kidney, one clip (2K, 1C) Goldblatt hypertensive and spontaneously hypertensive rats (SHR) compared with matched normotensive Wistar and Wistar-Kyoto (WKY) animals. The treatment was carried out for 1 month in Goldblatt-hypertensive rats and 3 months in SHR, i.e. for 1 month after blood pressure was normalized. At the end of the treatment period the passive mechanical properties of the isolated carotid artery were measured in situ. Carotid compliance was calculated from the pressure-volume relationship between 50 and 250 mmHg. Morphological parameters of the aortic wall, including medial thickness, nucleus density and elastin and collagen content, were recorded by an automated morphometric system. Renal and essential hypertension were associated with a shift of the passive pressure-volume relationship in the carotid, corresponding to a decrease in arterial compliance. The passive mechanical properties of the carotid were normalized by ACE inhibitor treatment in renovascular hypertensive rats but remained unchanged in chronically treated SHR. The ACE inhibitor completely reversed the medial hypertrophy in Goldblatt-hypertensive rats but the reversal of medial hypertrophy was incomplete in SHR. The elastin to collagen ratio in the aortic media was significantly increased by 3 months of treatment with the ACE inhibitor in the SHR and WKY groups but remained unchanged in the Goldblatt-hypertensive and Wistar rats treated for 1 month.
authors.affiliation: INSERM Unit 141, Hôpital Laribosière, Paris, France.
authors.forename: B I
authors.initials: BI
authors.lastname: Levy
authors.forename: J B
authors.initials: JB
authors.lastname: Michel
authors.forename: J L
authors.initials: JL
authors.lastname: Salzmann
authors.forename: M
authors.initials: M
authors.lastname: Azizi
authors.forename: P
authors.initials: P
authors.lastname: Poitevin
authors.forename: J P
authors.initials: JP
authors.lastname: Camilleri
authors.forename: M E
authors.initials: ME
authors.lastname: Safar
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D001158:Arteries / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D002339:Carotid Arteries / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D003187:Compliance; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000473:pathology / Q000503:physiopathology*; D007211:Indoles / Q000494:pharmacology*; D008297:Male; D020913:Perindopril; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D011921:Rats, Inbred WKY
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007211:Indoles; D020913:Perindopril