The fast nongenomic aldosterone effect on intracellular sodium ([Na+]i) and cell volume was studied by the fluorescent microscopy in isolated cortical part of collecting duct of the rat kidney (CCD). It was shown that aldosterone (10 nM) raised [Na+]i in hyposodium outer medium (14 mM). The rate of [Na+]i changes in response to external sodium shift (137-14 mM) twice as low in the presence of aldosterone (p < 0.05). Corticosterone (100 nM) was unable to simulate aldosterone effect. Similarly to sodium channel blocker amiloride (10(-5) M), protein kinase C (PKC) inhibitor RO-31-8220 (10(-7) M) abolished aldosterone effect. Aldosterone (10 nM) significantly decreased the amplitude and increased the characteristic time of the cell volume restoration in hypotonic medium of the rat principle cells (p < 0.001). Corticosterone (50 nM) was also unable to reproduce aldosterone effect. Amiloride (10(-5) M) did not significantly influence either the amplitude or the characteristic time of cell volume restoration during hypoosmotic challenge (p > 0.05). For the first time the specificity and important role of Ca(2+)-dependent kinase in the nongenomic aldosterone effects on ENaC activity and cell volume regulation in rat CCD were demonstrated.

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