Evidence for an enhanced transmembrane sodium (Na+) gradient induced by aldosterone in the incubated rat tail artery.

Aldosterone is known to stimulate Na+ transport as measured in terms of current-carrying capacity of epithelial sheets or of Na+ - K+ ATPase activity in cells. The possibility that this is reflected in an altered steady-state transmembrane Na+ distribution in vascular smooth muscle was here examined directly. Transmembrane Na+ and K+ gradients were first dissipated by overnight incubation in K-free physiological salt solution (PSS) at 10 degrees C and then reestablished by 3 hours in normal PSS at 37 degrees C. The addition of d-aldosterone (but not corticosterone) to these media significantly reduced cell Na. This involved only free cell Na which was reduced by about 20% of 3 mmole/kg dry wt. No significant change in membrane permeability measured in terms of net Li uptake at 3 degrees C or at 37 degrees C was observed. The lowest effective aldosterone concentration was 2.8 x 10(-9) M. These results are consistent with the observed enhancement of net Na+ transport in incubated arteries in DOCA-induced hypertension and in the SHR but do not account for the increased Na+ permeability observed in these states.