title: Blockade of angiotensin II type 1 receptors: effect on carotid and radial artery structure and function in hypertensive humans.
abstract: Converting-enzyme inhibition reduces cardiovascular hypertrophy in hypertensive subjects. Whether the blockade of angiotensin II type 1 (AT(1)) receptors reduces arterial hypertrophy has never been investigated. In a double-blind study versus placebo in subjects with essential hypertension, the effect of the AT(1) blocker irbesartan (150 mg/day for 8 weeks) on blood pressure, wall thickness, diameter and stiffness of the common carotid and radial arteries was studied, using echotracking techniques of high resolution. With irbesartan, mean blood pressure decreased significantly and proportionally to the baseline levels of active renin, and angiotensin I and II. There was a significant decrease in radial artery wall thickness. The percent change from baseline (+/- SEM) was -10.51 +/- 3.42 versus 6.18 +/- 4.77. There was no significant change in diameter or distensibility. This effect was correlated neither to blood pressure changes nor to hormonal baseline levels of the renin-angiotensin system. Carotid wall thickness and diameter were unchanged. Thus a 2-month treatment with an AT(1) antagonist significantly reduced radial but not carotid artery wall thickness. Blood pressure reduction could be explained on the basis of circulating renin-angiotensin activity. On the contrary, radial artery wall thickness reduction was independent of the baseline circulating renin-angiotensin activity and was not correlated with the effects of AT(1) blockade on blood pressure, thus implying the involvement of local hemodynamic and/or cellular mechanisms.
authors.affiliation: Department of Internal Medicine and INSERM (U337), Broussais Hospital, Paris, France.
authors.forename: A
authors.initials: A
authors.lastname: Benetos
authors.forename: S
authors.initials: S
authors.lastname: Gautier
authors.forename: A
authors.initials: A
authors.lastname: Laflèche
authors.forename: J
authors.initials: J
authors.lastname: Topouchian
authors.forename: G
authors.initials: G
authors.lastname: Frangin
authors.forename: X
authors.initials: X
authors.lastname: Girerd
authors.forename: J
authors.initials: J
authors.lastname: Sissmann
authors.forename: M E
authors.initials: ME
authors.lastname: Safar
mesh_terms: D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000803:Angiotensin I / Q000097:blood / Q000187:drug effects; D000804:Angiotensin II / Q000097:blood / Q000187:drug effects; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001713:Biphenyl Compounds / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D017534:Radial Artery / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D012083:Renin / Q000097:blood / Q000187:drug effects; D013777:Tetrazoles / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D013777:Tetrazoles; D000804:Angiotensin II; D000450:Aldosterone; D000803:Angiotensin I; D012083:Renin; D000077405:Irbesartan