ICEECE2012 Poster Presentations Adrenal cortex (113 abstracts)
Deletion of TASK3 K+ channels leads to hyperaldosteronism in neonatal mice
S. Bandulik 1 , P. Tauber 1 , D. Penton-Ribas 1 , I. Tegtmeier 1 , F. Lesage 2 , J. Barhanin 3 & R. Warth 1
1University of Regensburg, Regensburg, Germany; 2Université de Nice Sophia Antipolis, Valbonne, France; 3Université de Nice Sophia Antipolis, Nice Cedex, France.
Depolarisation of adrenal zona glomerulosa cells is a pivotal event for the secretion of aldosterone. Potassium channels like TASK1 and TASK3 are highly expressed in the adrenal cortex and determine the membrane voltage. Deletion of TASK3 K+ channels in mice caused a severe age-dependent hyperaldosteronism. The aim of this study was to identify the mechanisms underlying this phenotype.
Neonatal TASK3-/- mice (ko) showed higher plasma aldosterone levels compared to wildtype (wt) animals correlating with an increased adrenal mRNA expression level of the aldosterone-synthase. These high aldosterone levels decreased within the first two weeks of life. Plasma concentrations of progesterone and corticosterone showed the same age-dependent dysregulation. These results pointed to a broader adrenal dysfunction in newborn ko mice. A chip-based analysis was performed to measure differential gene expression in adrenals of 1 and 12 day old mice. Interestingly, adrenal renin mRNA was strongly upregulated in newborn ko mice, but decreased to normal wt levels in 12 day old mice. The high renin gene expression was confirmed by realtime PCR and by renin-specific immunofluorescence.
These data suggest that transient activation of the local adrenal renin-angiotensin-system contributes to the hyperaldosteronism of neonatal TASK3-/- mice. Future studies are needed to investigate the signalling pathways resulting in increased adrenal renin production and to identify the compensation mechanisms present in adult mice.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details unavailable.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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