The kidney is the primary organ ensuring K⁺ homeostasis. K⁺ is secreted into the urine in the distal tubule by two mechanisms: by the renal outer medullary K⁺ channel (K_ir1.1) and by the Ca²⁺-activated K⁺ channel (K_Ca1.1). Here, we report a novel knockout mouse of the β₂-subunit of the K_Ca1.1 channel (KCNMB2), which displays hyperaldosteronism after decreased renal K⁺ excretion. KCNMB2^−/− mice displayed hyperaldosteronism, normal plasma K⁺ concentration, and produced dilute urine with decreased K⁺ concentration. The normokalemia indicated that hyperaldosteronism did not result from primary aldosteronism. Activation of the renin-angiotensin-aldosterone system was also ruled out as renal renin mRNA expression was reduced in KCNMB2^−/− mice. Renal K⁺ excretion rates were similar in the two genotypes; however, KCNMB2^−/− mice required elevated plasma aldosterone to achieve K⁺ balance. Blockade of the mineralocorticoid receptor with eplerenone triggered mild hyperkalemia and unmasked reduced renal K⁺ excretion in KCNMB2^−/− mice. Knockout mice for the α-subunit of the K_Ca1.1 channel (KCNMA1^−/− mice) have hyperaldosteronism, are hypertensive, and lack flow-induced K⁺ secretion. KCNMB2^−/− mice share the phenotypic traits of normokalemia and hyperaldosteronism with KCNMA1^−/− mice but were normotensive and displayed intact flow-induced K⁺ secretion. Despite elevated plasma aldosterone, KNCMB2^−/− mice did not display salt-sensitive hypertension and were able to decrease plasma aldosterone on a high-Na⁺ diet, although plasma aldosterone remained elevated in KCNMB2^−/− mice. In summary, KCNMB2^−/− mice have a reduced ability to excrete K⁺ into the urine but achieve K⁺ balance through an aldosterone-mediated, β₂-independent mechanism. The phenotype of KCNMB2 mice was similar but milder than the phenotype of KCNMA1^−/− mice.