Obesity is a rapidly growing epidemic affecting >15% of the global adult population and has considerable clinical consequences and comorbidities, including hypertension, diabetes mellitus, cardiovascular and cerebrovascular diseases and chronic kidney disease. There is a strong association between obesity or body mass index and high blood pressure (BP) in epidemiological studies while the underlying pathophysiological events linking those conditions are not fully elucidated. Hypothetical mechanisms include a sedentary lifestyle and excess intake of processed foods that contribute to obesity, overactivation of the renin-angiotensin-aldosterone and sympathetic nervous systems, inflammation, altered adipokine homeostasis and the fatty kidney hypothesis involving adipose tissue accumulation in the renal sinus and perirenal space. There are multiple pharmacotherapeutic and surgical approaches for the management of obesity, including dual and triple agonist drugs targeting glucagon-like peptide-1, gastric inhibitory peptide and glucagon receptors and endoscopic bariatric procedures. Despite promising results with such therapeutic approaches in terms of body weight reduction and BP control, it is unclear whether such BP reduction may completely be attributable to weight loss. Confirmation of the adiposity dependence would lead to a major paradigm shift in our understanding of hypertension, potentially leading to a major shift in the causes of hypertension from primary hypertension to adiposity-dependent hypertension, leading to a shift from symptomatic treatment with antihypertensive medication to cause-focused treatment with weight loss medication. In this narrative review, the aim is to evaluate the potential pathophysiological mechanisms linking hypertension and obesity and the efficiency of potential therapeutic approaches on BP.