We summarized recent published literature regarding the influence of antihypertensive agents on uric acid level. Hyperuricemia is associated with risk for cardiovascular disease and death. However, the role of uric acid independent of established risk factor is uncertain. Recently researchers have drawn attention to a putative role of uric acid in pathogenesis of hypertension and renal disease. Uric acid levels are largely ignored in medical practice. An increase in serum uric acid levels has been observed during treatment with thiazide and loop diuretics and β-blockers, but treatment with β-blockers seems in most cases to be of no clinical importance. Calcium channel blockers have uricosuric effects, but decrease of uric acid level is not significant. Angiotensin converting enzymes inhibitors (ACE-I) and some of angiotensin II type 1 receptor antagonists (ARB) cause significant reduction of uric acid concentration. A feature of losartan that differentiates it from other ARB is its lowering in the largest degree of serum uric acid. Beyond typical mechanism for RAA blocking agents as hemodynamic renal blood flow increase and uric acid secretion, the losartan molecule is due to interfere with urate reabsorption in the renal proximal tubule.
The Losartan Intervention For Endpoint reduction in hypertension (LIFE) trial, which was designed to compare the effects of losartan and atenolol, has shown more clinical benefit during treatment with losartan. It is recommended that baseline uric acid level and antihypertensive treatment influence on uric acid concentration shoud be studied before starting and continuation of chosen antihypertensive therapy.