Moxonidine effect on microalbuminuria, thrombomodulin, and plasminogen activator inhibitor-1 levels in patients with essential hypertension

Increased sympathetic activity seems to play an important role in the patho genesis and development of complications of atherosclerotic origin in patie nts with essential hypertension (EH). The aim of this study was to evaluate the effect of a new antihypertensive agent, moxonidine (M), on microalbumi nuria (urine albumin excretion, UAE), plasma thrombomodulin (TM), and tissu e plasminogen activator inhibitor (PAI-1) in patients with mild to moderate EH associated with increased UAE. Fifty-eight patients (32 M, 26 F) with E H and microalbuminuria, with a mean age of 56.6 +/- 8.2 years and a body ma ss index (BMI) of 23.8 +/- 3.1 kg/m(2) who responded to M therapy (0.3-0.4 mg/daily) were studied before and after their blood pressure control. The 2 4-hour urine albumin excretion (RIA method), as well as TM and PAI-1 plasma levels (ELISA method), were determined before and 6 months after the initi ation of treatment under moxonidine therapy. At the end of the 6-month peri od, all patients remained normotensive. The 24-hour urine albumin excretion had decreased to 24.5 +/- 6.4 vs. 32.3 +/- 7.2 ug/min before therapy (P < 0.001). The plasma TM levels had decreased to 44.0 +/- 7 vs. 51.0 +/- 9 ng/ mL before therapy (P < 0.01), and PAI-I levels had also decreased to 11.5 /- 4.5 vs. 15.8 +/- 8 IU/mL before therapy (P < 0.05). The results of our s tudy suggest that in hypertensive patients with microalbuminuria, moxonidin e, an imidazoline I-1-receptor agonist, a new centrally acting antihyperten sive agent, significantly reduces urine albumin excretion as well as thromb omodulin and PAI-1 levels. These preliminary findings demonstrate a favorab le effect on renal function and endothelial homeostatic mechanisms (mainten ance of haemostatic balance).