Fosinopril decreases levels of soluble vascular cell adhesion molecule-1 in borderline hypertensive type II diabetic patients with microalbuminuria

Angiotensin converting enzyme inhibitors (ACE-I) are a mainstay for the tre atment of heart failure, and of diabetic microalbuminuria. Recently ACE-I h ave been found to decrease plasma levels of circulating vascular cell adhes ion molecule-1 (cVCAM-1) in patients with congestive heart failure. As incr eased cVCAM-1 levels are pathognomonic for diabetics with microangiopathy, we investigated the effects of ACE-I on plasma levels of cVCAM-2 intercellu lar adhesion molecule (cICAM-1), and cE-selectin in microalbuminuric diabet ics. In addition, the effects of ACE-I on plasma levels of plasminogen acti vator inhibitor (PAI-1) and of tissue plasminogen activator (TPA) were stud ied. Fosinopril (10 mg/day) was administered over 12 weeks to 11 microalbum inuric patients with non-insulin-dependent diabetes mellitus (NIDDM). As ex pected, baseline plasma concentrations of cE-selectin, cICAM-1, and cVCAM-1 were markedly higher in patients than in healthy control subjects (n = 82; P <.001). PAI-1 levels in NIDDM were similar to those in control subjects, whereas TPA levels were about 25% lower in patients than in control subjec ts (P =.013), Serum levels of cVCAM-1 decreased by -19% (CI: -25% to -13%) after treatment with fosinopril (P =.003) and were no longer different from those of the control group. In contrast, plasma levels of cE-selectin, cIC AM-1, PAI-1, and TPA were unaffected. As expected microalbuminuria decrease d by -44% (CI: -65 to -22; P =.004). In conclusion fosinopril lowered cVCAM -1 levels along with microalbuminuria in NIDDM. This may represent a novel mechanism of action of ACE-I in diabetes-associated endothelial dysfunction . Whether decreased VCAM-1 expression is responsible for the observed reduc tion in microalbuminuria, deserves further investigation. Am J Hypertens 19 99;12:217-222 (C) 1999 American Journal of Hypertension, Ltd.