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.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Bandulik S,Tauber P,Penton D,Schweda F,Tegtmeier I,Sterner C,Lalli E,Lesage F,Hartmann M,Barhanin J,Warth Rdoi
10.1210/en.2013-1101subject
Has Abstractpub_date
2013-08-01 00:00:00pages
2712-22issue
8eissn
0013-7227issn
1945-7170pii
en.2013-1101journal_volume
154pub_type
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