Despite a proven efficacy in lowering blood pressure, centrally acting
antihypertensive drugs are no longer widely used because of the relative high incidence of adverse effects. Most central side-effects occurring with these drugs are mediated by the alpha2-receptor.
Moxonidine is an
imidazoline receptor agonist that is highly selective for the I1-imidazoline receptor with little effect at the central alpha2-receptor.
Moxonidine has been shown to diminish sympathetic activity, as measured by
norepinephrine,
epinephrine and plasma
renin activity. Acute and long-term hemodynamic studies show that
moxonidine reduces arterial pressure by lowering systemic vascular resistance while sparing heart rate, cardiac output and stroke volume.
Moxonidine has been shown to reduce
left ventricular hypertrophy and is metabolically neutral; it may have a favourable effect on
insulin resistance. Clinical studies have documented efficacy of
moxonidine as an
antihypertensive agent. Most patients' blood pressure was satisfactorily controlled with a dose between 0.2 and 0.4 mg per day. Comparative studies are available with most other
antihypertensive drug classes, such as
clonidine,
diuretics, alpha-blockers, beta-blockers,
calcium antagonists, and
ACE inhibitors, and document similar blood pressure control with
moxonidine as with other agents. Specifically, by using 24-h ambulatory blood pressure monitoring, blood pressure control was found to be similar with
moxonidine and
enalapril. The side-effect profile of
moxonidine has been shown to be favorable as might be expected from its lack of an alpha2-receptor mediated central effect.
Moxonidine, therefore, represents an advance in the tolerability of anti-
adrenergic drugs without apparent reduction in efficacy. All of these observations suggest that
moxonidine may offer advantages over other
antihypertensive drugs, but clearly these potential advantages need to be properly evaluated in a prospective morbidity and mortality study.