Moxonidine: a new and versatile antihypertensive.

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.