Flow-mediated vasodilation and distensibility in relation to intima-media thickness of large arteries in mild essential hypertension

Whether endothelial dysfunction in essential hypertension is a cause or a c onsequence of structural vessel wall alterations is not known. The purpose of the present study was to compare flow-mediated vasodilation and mechanic al vessel wall properties of large arteries between never treated mild esse ntial hypertensive patients with normal intima-media thickness (IMT) and th ose exhibiting intima-media thickening. We measured brachial and carotid ar tery diameter and distension by Doppler frequency analysis of vessel wall m ovements in M-mode in ten essential hypertensive patients with normal carot id 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 di stal reactive hyperemia after 4 min of forearm occlusion. Nitroglycerin-med iated vasodilation was measured to assess endothelium-independent vasodilat ion, and BA blood flow was estimated using a pulsed Doppler system. Intima- media thickness of the carotid arteries was examined by high resolution B-m ode ultrasound. IMT was 0.66 +/- 0.02 mm in the HYP1 group, 0.84 +/- 0.03 m m in the HYP2 group (P < .01 v HYP1, P < .01 v CON), and 0.71 +/- 0.04 mm i n 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 now were not different between study groups. BA distension las well as carotid artery distension) was significantly lower i n the HYP1 group (52 +/- 6 mu m, P < .05 v CON), but not in the HYP2 group (72 +/- 10 mu m) when compared with the CON group (88 +/- 13 mu m). The dat a suggest that endothelial dysfunction and reduced distensibility of large arteries in patients with essential hypertension occur in the absence of st ructural vessel wall alterations. (C) 1999 American Journal of Hypertension , Ltd.