D. Rizzoni et al., ENDOTHELIAL DYSFUNCTION IN HYPERTENSION IS INDEPENDENT FROM THE ETIOLOGY AND FROM VASCULAR STRUCTURE, Hypertension, 31(1), 1998, pp. 335-341
The aim of our study was to evaluate the relationships between endothe
lial function, small resistance artery structure, and blood pressure i
n patients with primary or secondary hypertension. Sixty subjects were
included in the study: 9 patients with pheochromocytoma, 10 with prim
ary aldosteronism, 17 with renovascular hypertension, and 13 with esse
ntial hypertension with 11 normotensive subjects who served as control
s. Clinic and 24-hour ambulatory blood pressure (ABPM) were evaluated.
All subjects were submitted to a biopsy of subcutaneous fat. Small re
sistance arteries were dissected and mounted on a micromyograph and th
e media/lumen ratio was calculated. A dose-response curve to acetylcho
line was performed at cumulative concentrations from 10(-9) to 10(-5)
mol/L. The vasodilator response to acetylcholine was similarly impaire
d in the four groups of hypertensive patients (ANOVA P<.05 versus norm
otensive controls), without any significant difference among them, In
subcutaneous small arteries of patients with either primary aldosteron
ism or renovascular hypertension, a marked increase in media:lumen rat
io was observed, while in patients with pheochromocytoma, the extent o
f vascular structural alterations was similar to that observed in esse
ntial hypertension. No significant correlation between media-lumen rat
io or clinic blood pressure and maximum acetylcholine-induced vasodila
tation was observed. On the contrary, a significant, albeit not very c
lose, correlation between ABPM values and maximum acetylcholine-induce
d vasodilatation was observed (r=34, P<.05 with 24-hour systolic blood
pressure, r=0.36, P<.05 with 24-hour diastolic blood pressure). In co
nclusion, endothelial dysfunction seems to be independent from the deg
ree of vascular structural alterations and from the etiology of hypert
ension, and it is probably more linked to the hemodynamic load.