MOXONIDINE - A 2ND GENERATION OF CENTRALLY ACTING DRUGS - AN APPRAISAL OF CLINICAL-EXPERIENCE

The multifactorial etiology of hypertension is reflected in the various possible sites of therapeutic "attack" in the treatment of high blood pressure. A selective modulation of the sites in the central nervous system responsible physiologically for the regulation of blood pressure sounds promising. Moxonidine, an imidazoline, represents a new class of antihypertensives that acts via a recently discovered receptor, the I1-imidazoline receptor. Clinical experience is based on more than 2,000 patients and volunteers. Long-term efficacy was demonstrated in about 500 patients receiving a daily dose of 0.2-0.4 mg. Moxonidine behaves at least neutrally with regard to lipid or glucose metabolism as well as in concomitant diseases such as asthma. Regression of left ventricular hypertrophy within 3 months of treatment was an additional beneficial clinical effect. At the same time, catecholamine and renin plasma concentrations were decreased. A comparison with other well-established antihypertensive drugs such as nifedipine, atenolol, or angiotensin-converting enzyme inhibitors showed equieffectiveness in lowering blood pressure. The adverse events profile, however, always favored moxonidine. Moxonidine appears to dissociate between a very small alpha2-adrenoceptor action, reflecting side effects like sedation or dry mouth, and the specific antihypertensive action resulting from its selective putative agonistic effects at the I1-imidazoline receptor.