Dietary K

We previously reported that Na+-deprived mice lacking CAP1/Prss8 in kidney tubules maintained ENaC-mediated sodium balance albeit persistent hypoaldosteronism, hence indicating an uncoupling from aldosterone production. This further suggested an implication of the serine protease CAP1/Prss8 (prostasin) in the crosstalk of the kidney with the adrenal gland that does not express prostasin. When these knockout (Ko) mice were additionally exposed to a high K+ diet, plasma K+ levels and plasma aldosterone concentrations were normalized and no longer different from the control mice. The mRNA transcript expression of the adrenal aldosterone synthase Cyp11b2 that was lower in Na+-deprived CAP1/Prss8 Ko animals was in the normal range. Plasma aldosterone levels were similar to control animals indicating that K+ rescued the hypoaldosteronism in Na+-deprived CAP1/Prss8 Ko animals. These data suggest that CAP1/Prss8 (prostasin) is implicated in the regulation of aldosterone synthesis or production and that the consequences of CAP1/Prss8 deficiency can be compensated by high dietary K+ supplementation. Prostasin may therefore present a promising regulator of aldosterone production by affecting the adrenal steroidogenic pathway.