Hypertension (HTN), a globally prevalent non-communicable chronic disease (NCCD), is an international health concern. HTN has multifaceted pathogenesis with a varied prevalence across the globe. Excessive oxidative stress is the underlying cause of imbalance of the Renin Angiotensin Aldosterone System (RAAS) leading to elevated blood pressure (BP). Evidence-based medicine (EBM) along with suitable lifestyle modifications assists in managing the disease, lowering the risk of disease-associated cardiovascular morbidity and mortality. Losartan, an angiotensin receptor blocker (ARB), is one of the first-line drugs available. One of the complications of HTN is hyperuricemia, a metamorphosis in urate homeostasis. Studies have highlighted the uricosuric action of losartan along with its antihypertensive effects. However, varied therapeutic outcomes are observed in patients due to genetic polymorphisms based on different ethnical backgrounds. The present review focuses on the single nucleotide polymorphisms (SNPs) and the degree to which they affect losartan’s antihypertensive and serum uric acid (SUA) lowering effects.