Key result
Newborn Task3(-/-) mice displayed a severe adrenal phenotype with strongly increased plasma levels of aldosterone, corticosterone, and progesterone, accompanied by up-regulated adrenal renin expression.
Why the study?
Does Task3 gene knockout cause severe hyperaldosteronism and altered gene expression in neonatal mice?
Does Task3 gene knockout cause severe hyperaldosteronism and altered gene expression in neonatal mice?
Neonatal Task3 knockout mice exhibit severe hyperaldosteronism driven by activation of the local adrenal renin-angiotensin system, providing insights into mechanisms of hyperaldosteronism.
Suggests developmental role for TASK3 in aldosterone control; leaves open relevance to human primary aldosteronism.
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.
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Bandulik et al. (2013) studied Hyperaldosteronism. Task3 potassium channel knockout (neonatal) vs. Adult Task3(-/-) mice was evaluated on Adrenal phenotype and gene expression. Newborn Task3(-/-) mice displayed a severe adrenal phenotype with strongly increased plasma levels of aldosterone, corticosterone, and progesterone, accompanied by up-regulated adrenal renin expression.
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