Despite a proven efficacy in lowering blood pressure, centrally acting anti
hypertensive drugs are no longer widely used because of the relative high i
ncidence of adverse effects. Most central side-effects occurring with these
drugs are mediated by the alpha (2)-receptor, Moxonidine is an imidazoline
receptor agonist that is highly selective for the I-1-imidazoline receptor
with little effect at the central alpha (2)-receptor. Moxonidine has been
shown to diminish sympathetic activity, as measured by norepinephrine, epin
ephrine and plasma renin activity. Acute and long-term hemodynamic studies
show that moxonidine reduces arterial pressure by lowering systemic vascula
r resistance while sparing heart rate, cardiac output and stroke volume. Mo
xonidine has been shown to reduce left ventricular hypertrophy and is metab
olically neutral; it may have a favourable effect on insulin resistance. Cl
inical studies have documented efficacy of moxonidine as an antihypertensiv
e agent. Most patients' blood pressure was satisfactorily controlled with a
dose between 0.2 and 0.4 mg per day. Comparative studies are available wit
h most other antihypertensive drug classes, such as clonidine, diuretics, a
lpha -blockers, beta -blockers, calcium antagonists. and ACE inhibitors, an
d document similar blood pressure control with moxonidine as with other age
nts. Specifically, by using 24-h ambulatory blood pressure monitoring, bloo
d pressure control was found to be similar with moxonidine and enalapril. T
he side-effect profile of moxonidine has been shown to be favorable as migh
t be expected from its lack of an alpha (2)-receptor mediated central effec
t. Moxonidine, therefore, represents an advance in the tolerability of anti
-adrenergic drugs without apparent reduction in efficacy. All of these obse
rvations suggest that moxonidine may offer advantages over other antihypert
ensive drugs, but clearly these potential advantages need to be properly ev
aluated in a prospective morbidity and mortality study.