Potassium secretion may depend on the transport rate of Na, K‐ATPase in basolateral cell membranes of distal tubular cells. To examine this hypothesis experiments were performed in anaesthetized dogs during inhibition of proximal potassium reabsorption by acetazolamide or mannitol (fractional potassium excretion 1.2‐1.4) or additional stimulation of potassium secretion by ethacrynic acid (fractional potassium excretion 2.1). Ouabain in a dose which inhibits 70–80% of the Na, K‐ATPase activity reduced fractional potassium excretion to 0.8‐0.9 by an effect on distal tubular secretion since potassium transport in the proximal tubules was not affected. Ouabain‐sensitive potassium excretion varied in proportion to ouabain‐sensitive sodium reabsorption during variation in glomerular nitration rate, even at urinary sodium concentrations exceeding 80 mmol 1‐1. In experiments without ouabain, saline infusion raised potassium excretion and sodium reabsorption until maximal Na, K‐ATPase transport rate was reached, as judged from heat production measurements, but not during further increments in urine flow. After inhibition of Na, K‐ATPase activity by hypokalaemia, potassium excretion and cortical heat production remained constant over a wide range of urine flow and sodium excretion. We conclude that potassium secretion is dependent on intact Na, K‐ATPase activity and is stimulated by sodium delivery to the distal nephron until maximal transport rate of