Endothelial dysfunction in small resistance arteries of patients with non-insulin-dependent diabetes mellitus

Citation
D. Rizzoni et al., Endothelial dysfunction in small resistance arteries of patients with non-insulin-dependent diabetes mellitus, J HYPERTENS, 19(5), 2001, pp. 913-919
Citations number
36
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
0263-6352 → ACNP
Volume
19
Issue
5
Year of publication
2001
Pages
913 - 919
Database
ISI
SICI code
0263-6352(200105)19:5<913:EDISRA>2.0.ZU;2-1
Abstract
Objective Arterial hypertension is frequently associated with the presence of endothelial dysfunction in human subcutaneous small resistance arteries, as evaluated by responses to acetylcholine or bradykinin; however it is no t known whether patients with diabetes mellitus show similar alterations. T herefore, we have investigated endothelial function in subcutaneous arterie s of normotensive subjects (NT), of patients with essential hypertension (E H), of patients with non-insulin-dependent diabetes mellitus (NIDDM), as we ll as of patients with both essential hypertension and non-insulin-dependen t diabetes mellitus (NIDDM+EH). Patients and methods All subjects were submitted to a biopsy of the subcuta neous fat. Small arteries were dissected and mounted on a micromyograph. Th e media to lumen ratio (M/L) was calculated. A concentration-response curve to acetylcholine, to bradykinin as well as to the endothelium-independent vasodilator sodium nitroprusside were performed. We also evaluated the cont ractile response to endothelin-1. Intercellular adhesion molecule-1 (ICAM-1 ) and vascular cell adhesion molecule 1 (VCAM-1) plasma levels were also me asured. Results The vasodilatation to acetylcholine and bradykinin (but not to sodi um nitroprusside) was significantly and similarly reduced in EH, in NIDDM, and in NIDDM+EH compared with NT. The contractile response to endothelin-1 was similarly reduced in EH, in NIDDM and in NIDDM+EH. Plasma ICAM-1 and VC AM-1 concentrations were higher in EH, NIDDM and NIDDM+EH than in NT. Conclusions An evident endothelial dysfunction was detected in patients wit h NIDDM, and the simultaneous presence of EH did not seem to exert an addit ive effect. The contractile responses to endothelin-1 were reduced possibly as a consequence of ETA receptor downregulation. J Hypertens 19:913-919 (C ) 2001 Lippincott Williams & Wilkins.