Renal potassium elimination is tightly regulated in order to maintain electrolyte homeostasis under varying conditions. Here, we investigated the impact of aldosterone-dependent and - independent mechanisms of K+ excretion using adrenalectomized (ADX) mice as a tool. Under control conditions, absolute urinary K+ excretion was similar in control and ADX mice; however, under potassium-rich diet (HK) ADX mice had a reduced K+ tolerance. Renal K+ excretion consisted of an amiloride sensitive and insensitive portion and both were enhanced by HK in control and ADX mice. Interestingly, urinary K+ excretion capacity was not affected by varying the Na+ content of the diet. Aldosterone- responsive genes (alpha-ENaC, SGK1) and WNK4 were reduced in ADX mice; ROMK and MaxiK K+ channels were not changed. From the genes tested only SGK1 expression was augmented by HK in control and ADX mice. Immunofluorescence points at increased protein abundance of ROMK1 by HK in distal convoluted and connecting tubules of control but not of ADX mice. In summary, although ADX mice exhibit an aldosterone- independent way of K+ excretion, aldosterone is required for normal K+ excretion capacity. Immunofluorescence and realtime PCR suggest that in cortical distal nephron ROMK protein is increased by HK via non-transcriptional mechanisms.