Moxonidine is a new antihypertensive agent whose mechanism of action appear
s to involve specific stimulation of imidazoline receptors resulting in an
inhibition of the activity of the central and peripheral sympathetic nervou
s system. The drug seems to behave neutrally with respect to plasma lipid p
arameters. However, there are no data on the effects of moxonidine on the l
ow-density lipoprotein (LDL) subclass pattern or on the LDL oxidation susce
ptibility, both of which are known to play a prominent role in the pathogen
esis of atherosclerosis. Thus, we undertook the present study to examine th
e influence of moxonidine on the LDL subspecies profile and their susceptib
ility to copper-induced oxidative modification in 20 hypertensive patients
(11 men, 9 women) aged 38-61 years. Moxonidine administered at a dose of 0.
4 mg daily for 8 weeks produced a significant decrease in both systolic and
diastolic blood pressure (from 147 +/- 10 to 131 +/- 11 mm Hg, P < 0.001,
and from 98 +/- 4.5 to 86 +/- 5 mmHg, P < 0.001, respectively). No signific
ant change in plasma lipid profile was observed after moxonidine administra
tion. Additionally, no change in the susceptibility of LDL subclasses to co
pper-induced oxidative modification was noticed. Finally, drug therapy was
not followed by any change in either LDL phenotype or in mass and compositi
on of the three LDL subfractions. We conclude, that unlike other antihypert
ensive drugs, such as beta-blockers which may predispose to expression of a
relatively atherogenic lipoprotein subclass pattern, moxonidine does not a
ffect either plasma lipid parameters or lipoprotein composition.