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Endothelial dysfunction in hypertension is independent from the etiology and from vascular structure
D Rizzoni1, E Porteri, M Castellano
1Semeiotica and Metodologia Medica, University of Brescia, Italy. damiano.rizzoni@schering-pl.it
Insights
Endothelial dysfunction in hypertension is linked to hemodynamic load, not vascular structure or hypertension type. Ambulatory blood pressure measurements correlate with impaired vasodilator response in hypertensive patients.
Area of Science:
- Cardiovascular Medicine
- Hypertension Research
- Vascular Biology
Background:
- Endothelial dysfunction and vascular structural changes are key in hypertension.
- Understanding their relationship to different hypertension etiologies is crucial.
Purpose of the Study:
- To investigate the interplay between endothelial function, small resistance artery structure, and blood pressure in various hypertensive conditions.
- To compare these parameters across pheochromocytoma, primary aldosteronism, renovascular hypertension, and essential hypertension.
Main Methods:
- Sixty hypertensive patients and 11 controls underwent blood pressure monitoring (clinic and 24-hour ABPM).
- Subcutaneous small resistance arteries were analyzed for media/lumen ratio.
- Acetylcholine-induced vasodilation was assessed using micromyography.
Main Results:
- All hypertensive groups showed impaired vasodilator response compared to controls.
- Increased media/lumen ratio was noted in primary aldosteronism and renovascular hypertension.
- No correlation found between media/lumen ratio/clinic BP and vasodilation; significant correlation found between 24-hour ABPM and vasodilation.
Conclusions:
- Endothelial dysfunction in hypertension appears independent of vascular structural alterations and hypertension etiology.
- Hemodynamic load, particularly as reflected by ambulatory blood pressure, is more closely associated with endothelial dysfunction.
Abstract:
The aim of our study was to evaluate the relationships between endothelial function, small resistance artery structure, and blood pressure in patients with primary or secondary hypertension. Sixty subjects were included in the study: 9 patients with pheochromocytoma, 10 with primary aldosteronism, 17 with renovascular hypertension, and 13 with essential hypertension with 11 normotensive subjects who served as controls. Clinic and 24-hour ambulatory blood pressure (ABPM) were evaluated. All subjects were submitted to a biopsy of subcutaneous fat. Small resistance arteries were dissected and mounted on a micromyograph and the media/lumen ratio was calculated. A dose-response curve to acetylcholine was performed at cumulative concentrations from 10(-9) to 10(-5) mol/L. The vasodilator response to acetylcholine was similarly impaired in the four groups of hypertensive patients (ANOVA P<.05 versus normotensive controls), without any significant difference among them. In subcutaneous small arteries of patients with either primary aldosteronism or renovascular hypertension, a marked increase in media:lumen ratio was observed, while in patients with pheochromocytoma, the extent of vascular structural alterations was similar to that observed in essential hypertension. No significant correlation between media-lumen ratio or clinic blood pressure and maximum acetylcholine-induced vasodilatation was observed. On the contrary, a significant, albeit not very close, correlation between ABPM values and maximum acetylcholine-induced 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 conclusion, endothelial dysfunction seems to be independent from the degree of vascular structural alterations and from the etiology of hypertension, and it is probably more linked to the hemodynamic load.