Cg. Schalkwijk et al., ACE-inhibition modulates some endothelial functions in healthy subjects and in normotensive type I diabetic patients, EUR J CL IN, 30(10), 2000, pp. 853-860
Citations number
42
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Background The usefulness of treatment with an angiotensin-converting enzym
e-inhibitor (ACE-inhibitor) in normotensive patients with type 1 diabetes i
s controversial. We investigated whether ACE-inhibition improves endothelia
l function in such patients and compared the responses to those in healthy
subjects.
Design We studied 23 healthy volunteers (controls, aged 29.8 [SD 7.0] years
) and 24 type 1 diabetic patients (aged 28.7 [9.6] years; HbA(1c) 8.1 [1.2]
%; diabetes duration 13.8 [2-30] years; blood pressure < 140/90 mmHg; 7 wit
h microalbuminuria) after 5 weeks of ACE-inhibition (quinapril, 10 mg day(-
1)) and placebo in a randomized, double-blind cross-over design. Estimates
of endothelial function obtained were by flow-mediated vasodilation and pla
sma levels of endothelium-derived proteins.
Results As estimated from the measurements on placebo, type 1 diabetic pati
ents, as compared to the controls, had some impairment of endothelial funct
ion: plasma tissue-type plasminogen activator levels were lower (3.5 vs. 5.
4 ng mL(-1), P < 0.05), but there were no significant differences in brachi
al artery flow-mediated vasodilation or plasma levels of von Willebrand Fac
tor, endothelin-l, plasminogen activator inhibitor-1, soluble E-selectin or
vascular cell adhesion molecule-1. As compared to placebo, ACE-inhibition
increased flow-mediated vasodilation in controls (by 3.84% points [95% CI,
0.66 - 7.02], P < 0.05), but nor in type 1 diabetic patients (0.82% points
[95% CI, -2.72 - 4.36], P = 0.64; P = 0.08 vs. controls). On ACE-inhibition
soluble E-selectin levels decreased both in controls (from 43.0 to 37.0 ng
mL(-1), P < 0.01) and in type 1 diabetic patients (from 41.0 to 39.0 ng mL
(-1), P = 0.09). Other endothelial markers did not change during ACE-inhibi
tion.
Conclusion Normotensive type 1 diabetic patients with normoalbuminara or mi
croalbuminuria have mild endothelial dysfunction. Short-term ACE-inhibition
improves endothelial function as reflected by a decreased sE-selectin in h
ealthy subjects and in normotensive type I diabetic patients. In healthy su
bjects, ACE-inhibition increases flow-mediated vasodilation. In contrast, i
n type I diabetic patients, ACE-inhibition does not affect flow-mediated va
sodilation.