title: Flow-mediated vasodilation and distensibility in relation to intima-media thickness of large arteries in mild essential hypertension.
abstract: Whether endothelial dysfunction in essential hypertension is a cause or a consequence of structural vessel wall alterations is not known. The purpose of the present study was to compare flow-mediated vasodilation and mechanical vessel wall properties of large arteries between never treated mild essential hypertensive patients with normal intima-media thickness (IMT) and those exhibiting intima-media thickening. We measured brachial and carotid artery diameter and distension by Doppler frequency analysis of vessel wall movements in M-mode in ten essential hypertensive patients with normal carotid artery IMT (HYP1), in ten patients with increased IMT (HYP2), and in 13 normotensive control subjects (CON). Thereafter, we measured changes in brachial artery (BA) diameters during distal reactive hyperemia after 4 min of forearm occlusion. Nitroglycerin-mediated vasodilation was measured to assess endothelium-independent vasodilation, and BA blood flow was estimated using a pulsed Doppler system. Intima-media thickness of the carotid arteries was examined by high resolution B-mode ultrasound. IMT was 0.66 +/- 0.02 mm in the HYP1 group, 0.84 +/- 0.03 mm in the HYP2 group (P < .01 v HYP1, P < .01 v CON), and 0.71 +/- 0.04 mm in the CON group. Forearm occlusion was reduced in both the HYP1 group (3.4% +/- 3.6%, P < .01 v CON) and the HYP2 group (6.4% +/- 1.5%, P < .05 v CON) when compared with the CON group (16.5% +/- 2.8%). Nitroglycerin-mediated vasodilation and BA blood flow were not different between study groups. BA distension (as well as carotid artery distension) was significantly lower in the HYP1 group (52 +/- 6 microm, P < .05 v CON), but not in the HYP2 group (72 +/- 10 microm) when compared with the CON group (88 +/- 13 microm). The data suggest that endothelial dysfunction and reduced distensibility of large arteries in patients with essential hypertension occur in the absence of structural vessel wall alterations.
authors.affiliation: Department of Internal Medicine D, University of Münster, Germany. hausber@uni-muenster.de
authors.forename: M
authors.initials: M
authors.lastname: Barenbrock
authors.forename: M
authors.initials: M
authors.lastname: Hausberg
authors.forename: M
authors.initials: M
authors.lastname: Kosch
authors.forename: S A
authors.initials: SA
authors.lastname: Golubev
authors.forename: K
authors.initials: K
authors.lastname: Kisters
authors.forename: K H
authors.initials: KH
authors.lastname: Rahn
mesh_terms: D000328:Adult; D001916:Brachial Artery / Q000473:pathology*; D002339:Carotid Arteries / Q000473:pathology*; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000494:pharmacology; D017539:Tunica Intima / Q000473:pathology*; D014664:Vasodilation
chemical_list: D005996:Nitroglycerin