Losartan Potassium Oral Administration Decreased Intraocular Pressure in Humans A Pilot Study Ciro Costagliola, 1 Marco Verolino, 1 Gennarfrancesco Iaccarino, 1 Maria Leonarda De Rosa, 2 Marco Ciancaglini 3 and Leonardo Mastropasqua 3 1 Istituto di Clinica Oculistica, II Università degli Studi di Napoli, Napoli, Italy 2 Cattedra di Geriatria, Università degli Studi di Napoli ‘Federico II’, Napoli, Italy 3 Istituto di Clinica Oculistica, Università degli Studi di Chieti, Chieti, Italy SHORT COMMUNICATION Clin Drug Invest 1999 Apr; 17 (4): 329-332 1173-2563/99/0004-0329/$02.00/0 © Adis International Limited. All rights reserved. Losartan potassium is an orally active, nonpep- tide, angiotensin II receptor antagonist. [1] Chemi- cally, it is a biphenyl tetrazole that is converted in vivo to an active, carboxylic acid metabolite, E-3174. [2] This novel agent binds competitively and selectively to the AII subtype I (AT1) receptor, thereby blocking AII-induced physiological effects. [3] Its active metabolite, being a noncompet- itive antagonist with an affinity for the AT1 recep- tor 10-fold greater than its parent compound, con- tributes to the antihypertensive effect of losartan, which persists throughout 24 hours after once- daily administration. [3,4] Ramirez and co-workers, [5] demonstrated in rabbits the presence of the precursor and enzymes necessary for angiotensin II generation in the eye, and suggested that the eye contains a local renin- angiotensin system, with physiological and patho- physiological implications. Recently, Costagliola and co-workers [6] demonstrated that captopril, an angiotensin converting enzyme inhibitor, was able to reduce intraocular pressure (IOP) in normal subjects and in patients with primary open-angle glaucoma. [6] These findings suggested that ocular angiotensin II might be involved in the regulation of IOP and that the inhibition of ocular angiotensin II receptors might be a means of reducing it. The aim of this study was to verify the effects of losartan potassium on IOP in control subjects and in patients with essential arterial hypertension, to assess adverse effects (if any), and to ascertain its possible mechanism of action. Preliminary re- sults have been reported elsewhere. [7] Patients and Methods The clinical trial included 20 participants (10 men and 10 women, aged from 40 to 55 years) divided into two age- and gender-matched groups as follows: group A, 10 patients with arterial hyper- tension, on therapy (α- and β-blockers, ACE inhi- bitors); group B, 10 healthy volunteers (table I). All participants received a detailed physical and ophthalmological examination. Patients with systemic diseases other than arte- rial hypertension, those with aphakia or visual acu- ity less than 20/200 in either eye, those wearing Table I. Demographic characteristics of study population Control (volunteers) Patients with hypertension Total no. cases 10 10 Total no. of eyes 10 10 Gender (M/F) 5/5 5/5 Age range (y) 40-55 40-55 Diagnosis of patients treated Healthy volunteers Arterial hypertension Mean entry IOP (mm Hg) 15.5 15.6 Mean entry SBP (mm Hg) 125 175 Mean entry DBP (mm Hg) 80 80 Duration of treatment (h) 6 6 DBP = diastolic blood pressure; IOP = intraocular pressure; SBP = systolic blood pressure.