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cGMP‐dependent protein kinase II and aldosterone secretion
Author(s) -
Spießberger Beate,
Bernhard Dominik,
Herrmann Stefan,
Feil Susanne,
Werner Claudia,
Luppa Peter B.,
Hofmann Franz
Publication year - 2009
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2008.06839.x
Subject(s) - secretion , aldosterone , protein kinase a , cgmp dependent protein kinase , chemistry , endocrinology , medicine , kinase , microbiology and biotechnology , mitogen activated protein kinase kinase , biology , biochemistry
ACTH‐stimulated aldosterone secretion can be inhibited by atrio‐natriuretic peptide/cGMP. The mechanism behind this modulation has been reported to involve cGMP‐dependent activation of phosphodiesterase 2 (PDE2) and hydrolysis of cAMP. Recently it was reported that activation of cGMP‐dependent protein kinase II (cGKII) stimulated aldosterone secretion in rat zona glomerulosa cells. The zona glomerulosa of the murine adrenal cortex expresses cGKII and PDE2. We used mice with a homozygous inactivation of the cGKII gene to investigate in vivo the potential role of this kinase in aldosterone secretion. Basal plasma renin and aldosterone levels were similar in wild‐type and cGKII −/− mice. In vivo injection of atrio‐natriuretic peptide decreased ACTH‐stimulated aldosterone secretion in wild‐type mice, but had no effect in cGKII‐deficient mice. These results support the view that cGKII modulates aldosterone secretion in the murine adrenal cortex.