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Previous  in vitro  studies demonstrated that aldosterone rapidly activates sodium-hydrogen exchangers 1 and 3 (NHE 1 and 3).  In vitro  investigations revealed that protein kinase C (PKC) regulates NHE properties. We previously demonstrated that aldosterone rapidly enhances PKC α  protein abundance in the rat kidney. There are no reports of renal PKC β  (I and II) protein levels related to the regulation by aldosterone. There are also no  in vivo  data regarding the rapid effects of aldosterone on renal protein levels of NHE (1 and 3) and PKC β  (I and II), simultaneously. In the current study, rats received normal saline solution or aldosterone (150  μ g/kg BW, i.p.). After 30 minutes, abundance and immunoreactivity of these proteins were determined by Western blot analysis and immunohistochemistry, respectively. Aldosterone increased NHE1 and NHE3 protein abundance to 152% and 134%, respectively ( P  < 0.05). PKC β I protein level was enhanced by 30%, whereas PKC β II declined slightly. Aldosterone increased NHE protein expression mostly in the medulla. PKC β I immunostaining intensity was increased in the glomeruli, renal vasculature, and thin limb of the loop of Henle, while PKC β II was reduced. This is the first  in vivo  study to simultaneously demonstrate that aldosterone rapidly elevates PKC β I and NHE (1 and 3) protein abundance in the rat kidney. Aldosterone-induced NHE (1 and 3) protein levels may be related to PKC β I activation.

Rapid Action of Aldosterone on Protein Levels of Sodium-Hydrogen Exchangers and Protein Kinase C Beta Isoforms in Rat Kidney