In the cauda epididymidis, sodium chloride is reabsorbed isotonically with water and potassium is secreted into the ductal lumen (Wong & Yeung, 1977, 1978; these transport processes seem to have many characteristics typical of the processes occurring in the distal tubule of the kidney. Apart from electrolyte and water transport, proteins are also secreted into the ductal lumen. The epididymal epithelium actively maintains a definite milieu within the tubule in which the spermatozoa are maturing. In several transporting epithelia such as those of the toad bladder, frog skin, salivary and sweat glands, intestine and renal tubule (for references, see Hierholzer, Wiederholt & Stolte, 1966), active sodium transport is regulated by the adrenocortical hormones. This study was designed to investigate the role of the adrenal glands in regulating salt and water transport in the epididymis. Net sodium and water fluxes across the perfused rat cauda epididymidis were measured in normal and adrenalectomized rats and adrenalectomized rats injected with adrenocortical hormones.Thirty fertile Sprague-Dawley rats (350-450 g) were bilaterally adrenalectomized under sodium pentobarbitone (50 mg/kg body weight) anaesthesia and then given 1% NaCl solution instead of drinking water. After 3 days, eight rats were injected with D-aldosterone (i.p., 75 µg kg-1 day-1), eighkrats received cortisol (Efcortelan, i.p., 16 mg kg-1 day-1) and a further six rats received D-aldosterone+cortisol for 4 days before the experiment. The remaining eight animals received no further treatment.Sodium and water transport across the perfused rat cauda epididymidis were measured by the method described previously (Wong & Yeung, 1978). The cauda epididymidis (about 18 cm long) was perfused with Krebs bicarbonate solution (containing 118 mM-NaCl, 4-7 mM-KCl, 2-56 mM-CaCl2, 1-13 mM-MgS04, 1-17 mM-NaH2P04 and 25 mM-NaHC03, pH 7-4) and subsequently with solutions containing various concentrations of sodium (NaCl was replaced by choline chloride). Sodium reabsorption altered in a curvilinear manner with the concentration of sodium in the luminal fluid, with an apparent Km of about 20 mM-Na+ (Fig. la). In rats adrenalectomized for 7 days, sodium reabsorption was undetectable between 0 and 70 mM-Na+ and the rate measured at 143 mM-Na+ was de¬ pressed by about 50% compared with untreated controls (jP<0-001, Student's i-test). Injection of D-aldosterone for 4 days partially (about 40%) restored the rate of sodium reabsorption; values were significantly higher than those measured in adrenalectomized rats with the concentration of sodium between 25 and 70 mmol/1 (P<0-01). However, injection of cortisol had little if any effect on Na+ reabsorption; when D-aldosterone and cortisol were given together values were not significantly different from those observed after administration of D-aldosterone alone.