title: Regression of hypertension-induced vascular hypertrophy by an ACE inhibitor and calcium antagonist in the spontaneously hypertensive rat.
abstract: This study was designed to investigate the effects of antihypertensive drugs on vascular hypertrophy and vascular angiotensin II in vivo in spontaneously hypertensive rats (SHR). Hydralazine (10 mg/kg/day), delapril (angiotensin converting enzyme inhibitor; 20 mg/kg/day), manidipine (calcium channel blocker; 10 mg/kg/day), and vehicle were given by gavage to four groups of SHR between 4 and 5 months of age. The aortic angiotensin II level was measured by highly sensitive radioimmunoassay coupled with high pressure liquid chromatography; aortic morphologic studies were performed. Each drug treatment effectively lowered blood pressure to the same level. However, the aortic wall thickness, medial-intimal areas, and wall to lumen ratio of abdominal aorta decreased significantly (p < 0.05, p < 0.01, p < 0.01, respectively) with delapril and manidipine but not hydralazine. Delapril significantly decreased aortic angiotensin II levels (p < 0.05), whereas manidipine treatment significantly increased them (p < 0.05). The aortic angiotensin II level was not changed by hydralazine. These results show that delapril and manidipine caused regression of hypertension-induced vascular hypertrophy in SHR. The probable mechanism of regression of aortic hypertrophy by delapril was inhibition of vascular angiotensin II formation, but the mechanism for manidipine was unclear.
authors.affiliation: Department of Geriatric Medicine, Osaka University Medical School, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Morishita
authors.forename: J
authors.initials: J
authors.lastname: Higaki
authors.forename: F
authors.initials: F
authors.lastname: Nakamura
authors.forename: N
authors.initials: N
authors.lastname: Tomita
authors.forename: H
authors.initials: H
authors.lastname: Yu
authors.forename: M
authors.initials: M
authors.lastname: Nagano
authors.forename: H
authors.initials: H
authors.lastname: Mikami
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001012:Aorta, Abdominal / Q000187:drug effects / Q000473:pathology* / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004095:Dihydropyridines / Q000494:pharmacology; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy*; D006984:Hypertrophy / Q000188:drug therapy / Q000209:etiology; D007189:Indans / Q000494:pharmacology; D008297:Male; D009578:Nitrobenzenes; D010879:Piperazines; D051381:Rats; D011918:Rats, Inbred SHR; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D007189:Indans; D009578:Nitrobenzenes; D010879:Piperazines; D000804:Angiotensin II; D006830:Hydralazine; C054218:manidipine; C047759:delapril