ENDOTHELIAL DYSFUNCTION IN HYPERTENSION IS INDEPENDENT FROM THE ETIOLOGY AND FROM VASCULAR STRUCTURE

Citation
D. Rizzoni et al., ENDOTHELIAL DYSFUNCTION IN HYPERTENSION IS INDEPENDENT FROM THE ETIOLOGY AND FROM VASCULAR STRUCTURE, Hypertension, 31(1), 1998, pp. 335-341
Citations number
25
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
0194911X
Volume
31
Issue
1
Year of publication
1998
Part
2
Supplement
S
Pages
335 - 341
Database
ISI
SICI code
0194-911X(1998)31:1<335:EDIHII>2.0.ZU;2-R
Abstract
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.