Previous in vitro studies demonstrated that aldosterone rapidly activates sodium-hydrogen exchangers 1 and 3 (NHE 1 and 3). In\nvitro investigations revealed that protein kinase C (PKC) regulates NHE properties. We previously demonstrated that aldosterone\nrapidly enhances PKC�± protein abundance in the rat kidney. There are no reports of renal PKC�² (I and II) protein levels related to\nthe regulation by aldosterone. There are also no in vivo data regarding the rapid effects of aldosterone on renal protein levels of NHE\n(1 and 3) and PKC�² (I and II), simultaneously. In the current study, rats received normal saline solution or aldosterone (150 �¼g/kg\nBW, i.p.). After 30 minutes, abundance and immunoreactivity of these proteins were determined by Western blot analysis and\nimmunohistochemistry, respectively. Aldosterone increased NHE1 and NHE3 protein abundance to 152% and 134%,\nrespectively (P < 0 05). PKC�²I protein level was enhanced by 30%, whereas PKC�²II declined slightly. Aldosterone increased\nNHE protein expression mostly in the medulla. PKC�²I immunostaining intensity was increased in the glomeruli, renal\nvasculature, and thin limb of the loop of Henle, while PKC�²II was reduced. This is the first in vivo study to simultaneously\ndemonstrate that aldosterone rapidly elevates PKC�²I and NHE (1 and 3) protein abundance in the rat kidney. Aldosteroneinduced\nNHE (1 and 3) protein levels may be related to PKC�²I activation.
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