Adrenergic mechanisms and remodeling of subcutaneous small resistance arteries in humans.
BACKGROUND
Vascular structural alterations in small resistance arteries of patients with essential hypertension (EH) are mostly characterized by inward eutrophic remodeling. In fact, no difference in the smooth muscle cell volume (CV) between normotensive subjects (NT) and essential hypertensive patients was observed. However, experimental models of hypertension with chronic infusion of agonists of adrenergic receptors were characterized by the presence of smooth muscle cell hypertrophy or hyperplasia. Recently, we have observed the presence of vascular smooth muscle cell hypertrophy in patients with renovascular hypertension.


OBJECTIVE
The aim of the study to investigate the structural characteristics of subcutaneous small resistance arteries of NT, of EH, and of patients with phaeochromocytoma (Phaeo).


METHODS
Thirty Phaeo, 30 NT and 30 EH were included in the study. A biopsy of subcutaneous fat was taken from all subjects. Small resistance arteries (relaxed diameter 160-280 microm) were dissected and mounted on a micromyograph and the media : lumen ratio was calculated. In nine Phaeo, nine NT and 13 EH the cell volume was measured by an unbiased stereological principle, the 'disector' method. RESULTS No difference in smooth muscle cell volume was observed between groups. However, inward remodeling in Phaeo was less marked than in EH, although the increase in media : lumen ratio was similar compared with NT. However, the lack of changes in media cross-sectional area, compared with NT, suggest that there has been little hypertrophy, the changes observed thus being eutrophic.


CONCLUSIONS
Our data show, based on a reasonably large sample, that a pronounced activation of the adrenergic system is not associated with vascular smooth muscle cell hypertrophy or hyperplasia in humans. It is therefore possible that adrenergic mechanisms may have a relevant role in the development of eutrophic remodeling in small vessels.
Porteri
Enzo
E
Department of Medical and Surgical Sciences, University of Brescia, Italy.
Rizzoni
Damiano
D
Mulvany
Michael John
MJ
De Ciuceis
Carolina
C
Sleiman
Intissar
I
Boari
Gianluca E
GE
Castellano
Maurizio
M
Muiesan
Maria Lorenza
ML
Zani
Francesca
F
Rosei
Enrico Agabiti
EA
D000310:Adrenal Gland Neoplasms / Q000503:physiopathology* / Q000601:surgery; D000315:Adrenalectomy; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001158:Arteries / Q000503:physiopathology* / Q000601:surgery; D015415:Biomarkers / Q000652:urine; D001794:Blood Pressure / Q000502:physiology; D018660:Blood Pressure Monitoring, Ambulatory; D048429:Cell Size / Q000502:physiology; D002940:Circadian Rhythm / Q000502:physiology; D003971:Diastole / Q000502:physiology; D004548:Elasticity; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism / Q000503:physiopathology; D004837:Epinephrine / Q000652:urine; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000473:pathology; D009638:Norepinephrine / Q000652:urine; D010673:Pheochromocytoma / Q000503:physiopathology* / Q000601:surgery; D013599:Systole / Q000502:physiology; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000502:physiology*
D000959:Antihypertensive Agents; D015415:Biomarkers; D009638:Norepinephrine; D004837:Epinephrine