Task3 Potassium Channel Gene Invalidation Causes Low Renin and Salt-Sensitive Arterial Hypertension

• DOI: 10.1210/en.2012-1527
• Publication Date: 2012-09-21T17:45:03Z
• Authors: David Penton; Sascha Bandulik; Frank Schweda; Sophia Haubs; Philipp Tauber; Markus Reichold; Lu Dang Cong; Abeer El Wakil; Thomas Budde; Florian Lesage; Enzo Lalli; Maria-Christina Z...; Richard Warth; Jacques Barhanin
• Keywords: Mice, Knockout; 0301 basic medicine; 0303 health sciences; [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology; Potassium Channels; Blood Pressure; Adaptation, Physiological; Mice; 03 medical and health sciences; Phenotype; Adrenal Glands; Hypertension; Renin; Animals; Calcium; Zona Glomerulosa; Sodium Chloride, Dietary; Aldosterone; Cells, Cultured

Task1 and Task3 potassium channels (Task: tandem of P domains in a weak inward rectifying K(+) channel-related acid-sensitive channel) are believed to control the membrane voltage aldosterone-producing adrenal glomerulosa cells. This study aimed at understanding role for aldosterone secretion. The phenotype Task3(-/-) mice was investigated using electrophysiology, slices, blood pressure measurements. Primary adrenocortical cells were strongly depolarized compared with wild-type (-52 vs. -79 mV), fresh slices Ca(2+) signaling abnormal. In living mice, regulation secretion showed specific deficits: Under low Na(+) high diets, protocols known increase aldosterone, under standard diet, inactivation compensated normal. However, two lower failed mice. physiological disturbed: aldosterone-renin ratio, an indicator autonomous secretion, 3-fold elevated diets. Isolated glands produced 2-fold more aldosterone. As consequence, salt-sensitive arterial hypertension (plus 10 mm Hg). conclusion, plays important adaptation dietary salt intake.