The secretion of aldosterone by glomerulosa cells is tightly controlled to adjust salt excretion to salt intake. Pivotal for the stimulation of aldosterone production by angiotensin II and high plasma K+ is the depolarization of the cell membrane. Activity of 2-P-domain potassium channels TASK1, TASK3, and TREK1 is important for the control of the membrane voltage. This study aimed at investigating the particular contribution of TASK3 potassium channel for the regulation of aldosterone production. Plasma aldosterone under various salt diets was compared in wildtype and TASK3 knockout mice. In addition, aldosterone secretion of isolated adrenal glands was analyzed. The deletion of TASK3 led to slight changes of the K⁺ sensitivity of the aldosterone secretion. In ex vivo experiments using isolated adrenal glands, also small changes of the kinetics of aldosterone secretion were observed. Analyzing the expression pattern of TASK3 in wildtype mice by immunofluorescence, we found TASK3 expressed in the zona glomerulosa and to lesser extent in the zona fasciculata. These data are suggestive for a role of TASK3 in the control of aldosterone secretion in mice and they could have implications for human disorders linked to pathological aldosterone secretion.