Why the study?
Does atrio-natriuretic peptide inhibit ACTH-stimulated aldosterone secretion via cGMP-dependent protein kinase II in mice?
Does atrio-natriuretic peptide inhibit ACTH-stimulated aldosterone secretion via cGMP-dependent protein kinase II in mice?
The study demonstrates that cGMP-dependent protein kinase II (cGKII) is required for atrio-natriuretic peptide-mediated inhibition of ACTH-stimulated aldosterone secretion in mice.
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ANP inhibition of ACTH-stimulated aldosterone requires cGKII in mice; leaves open relevance to human physiology or therapy.
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.
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Spießberger et al. (2009) studied this question.
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