Referenced in: none

Automatically associated channels: SK3 , TASK1 , TASK3

Title: Severe hyperaldosteronism in neonatal Task3 potassium channel knockout mice is associated with activation of the intraadrenal renin-angiotensin system.

Authors: Sascha Bandulik, Philipp Tauber, David Penton, Frank Schweda, Ines Tegtmeier, Christina Sterner, Enzo Lalli, Florian Lesage, Michaela Hartmann, Jacques Barhanin, Richard Warth

Journal, date & volume: Endocrinology, 2013 Aug , 154, 2712-22

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/23698720

Abstract
Task3 K(+) channels are highly expressed in the adrenal cortex and contribute to the angiotensin II and K(+) sensitivity of aldosterone-producing glomerulosa cells. Adult Task3(-/-) mice display a partially autonomous aldosterone secretion, subclinical hyperaldosteronism, and salt-sensitive hypertension. Here, we investigated the age dependence of the adrenal phenotype of Task3(-/-) mice. Compared with adults, newborn Task3(-/-) mice displayed a severe adrenal phenotype with strongly increased plasma levels of aldosterone, corticosterone, and progesterone. This adrenocortical dysfunction was accompanied by a modified gene expression profile. The most strongly up-regulated gene was the protease renin. Real-time PCR corroborated the strong increase in adrenal renin expression, and immunofluorescence revealed renin-expressing cells in the zona fasciculata. Together with additional factors, activation of the local adrenal renin system is probably causative for the severely disturbed steroid hormone secretion of neonatal Task3(-/-) mice. The changes in gene expression patterns of neonatal Task3(-/-) mice could also be relevant for other forms of hyperaldosteronism.