SAT-363 Deletion of TASK Channels Selectively from the Zona Glomerulosa Causes Mild Angiotensin II-Independent Hyperaldosteronism with Elevated Blood Pressure in Mice

Overt dysregulation of the renin-angiotensin-aldosterone system (primary aldosteronism: APA and IHA) has long been known for its deleterious cardiovascular consequences. Recently, however, subclinical mild hyperaldosteronism was recognized as a significant risk factor for hypertension, and may represent an early stage in the disease spectrum. Previously, we developed mouse models of hyperaldosteronism by globally deleting subunits of the TWIK-related acid sensitive potassium channel (TASK). Global TASK-1 (Kcnk3) and TASK-3 (Kcnk9) KO mice markedly overproduce Ang II-independent (autonomous) aldosterone, that is not suppressed by high dietary sodium and is accompanied by low renin and elevated blood pressure. Here, we report a novel mouse model of mild hyperaldosteronism produced by the zona glomerulosa (zG)-specific deletion of TASK channels. To generate trigenic Cyp11b2Cre …