A crucial mechanism to control sodium homeostasis and arterial blood pressure is seen in the modulation of the sodium reabsorption along the renal nephron. The ultimate regulation occurs at the apical surface of the collecting ducts and is mediated by the amiloride sensitive epithelial sodium channel (ENaC). Inherited alterations in channel structure, which induce abnormalities in function, have been recognised to play a major role in the hypertension observed in patients with Liddle's syndrome and salt-wasting which coincides with some variants of pseudohypoaldosteronism. In most tissues the channel is formed by three homologue subunits (a, b, [gamma]). The expression, stoichiometry and activity of ENaC in response to various stimuli is differentially regulated and complex. Induction of the renal ENaC by sodium restriction is well accepted, however, very limited information exists about its role during the onset of renovascular hypertension. Therefore, the present study determines the responses of renal ENaC subunits mRNA to well defined (±1mmHg) 24h- reductions in renal perfusion pressure (rRPP). A pressure dependent increase of a-ENaC-mRNA levels was obeserved at rRPP<90mmHg. rRPP-oscillations (0.1Hz) or a high sodium diet abolished this effect at low rRPP.