<p>Hypertension is the leading contributor to premature death and disability in the world. Genetic susceptibility and high dietary salt (NaCl) consumption have long been considered to be the primary culprits but growing evidence indicates that low dietary potassium consumption has an equally important role. Although the underlying mechanisms are complex and multifactorial, the potassium switch signalling mechanism in the kidney distal convoluted tubule represents a crucial pathway with implications for preventing and treating hypertension. Comprising a Kir4.1 and Kir5.1 channel potassium-sensing mechanism, a WNK kinase-induced phosphorylation cascade, and the thiazide-diuretic-targeted sodium chloride co-transporter, the potassium switch orchestrates a physiological response in the distal nephron that maintains sodium–potassium balance over wide variations in dietary potassium intake. The potassium switch is ideally adapted for the low-salt, feast-and-famine diets of hunter-gatherers. However, low potassium consumption, which is common in high-sodium modern diets, promotes potassium conservation at the expense of increasing sodium reabsorption, exacerbating salt-sensitive hypertension and its associated cardiovascular complications. Here, we discuss current understanding of the potassium switch and how its role in kidney adaptation to the modern diet can contribute to hypertension.</p>