Abstract:
BACKGROUND:Hypertension and other vascular diseases are more prevalent in diabetic patients than in the general population. In humans and in several animal models of diabetes, a disturbance of endothelium-dependent responses has been shown. Oxyhemoglobin is one of the most known modulators of these endothelium-dependent responses. We postulate that high levels of plasmatic glycosylated hemoglobin, a frequent profile in diabetic patients, may be the cause of the disturbance in endothelium-dependent relaxation and/or contraction. METHODS AND RESULTS:Endothelium-dependent responses to acetylcholine and several alpha-adrenergic agonists (norepinephrine, methoxamine, and clonidine) were tested in segments of rat aorta. Experiments were carried out in control segments and in those preincubated with several concentrations of nonglycosylated, low-glycosylated (7.3%), and high-glycosylated (14%) human hemoglobin. Low concentrations of high-glycosylated human hemoglobin (1 to 100 nmol/L) but not of low- or nonglycosylated hemoglobin, inhibited endothelium-dependent relaxation caused by acetylcholine in intact vessels. The same effect was observed on relaxations caused by nitric oxide in denuded ones. High-glycosylated human hemoglobin (10 nmol/L) induced an increase in norepinephrine-evoked contraction in intact vessels; this latter effect was also shown in vessels contracted with methoxamine but not with clonidine. De-endothelialization of the vascular segments blunted these effects of high-glycosylated human hemoglobin. CONCLUSIONS:High glycosylation of human hemoglobin impairs endothelium-mediated vasoactive responses and may play a pathophysiological role in producing hypertension and vascular diseases in diabetic patients.
journal_name
Circulationjournal_title
Circulationauthors
Rodríguez-Mañas L,Arribas S,Girón C,Villamor J,Sánchez-Ferrer CF,Marín Jdoi
10.1161/01.cir.88.5.2111subject
Has Abstractpub_date
1993-11-01 00:00:00pages
2111-6issue
5 Pt 1eissn
0009-7322issn
1524-4539journal_volume
88pub_type
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