In order to examine if modulation by vasopressin of NaCl transport in Henle's loops (via V2 receptors) can significantly modify medullary ionic hypertonicity, the effects of stimulation or inhibition of these receptors were studied in anaesthetized Wistar rats. Total electrolyte concentration in the medullary interstitium was continuously measured as tissue admittance (reciprocal impedance), using needle electrodes recording from the inner and outer medulla of the in situ kidney. Deamino-[Cys1, D-Arg8]vasopressin (dDAVP], a V2 agonist, infused i.v. at 7.5 ng.min-1.kg-1, significantly increased admittance by 9% and 8% in the inner and outer medulla, respectively. A slightly pressor i.v. infusion of natural arginine vasopressin (AVP) induced pressure natriuresis and did not affect medullary electrolyte concentration. Inhibition of V2 receptors with [d(CH2)5, D-Phe2, Ile4]-AVP, infused i.v. at 133 micrograms.h-1 kg-1 in indomethacin-treated rats, decreased admittance (significant in the inner medulla). Neither of the three agents used caused significant changes in the renal blood flow (RBF) or clearance of inulin (Cin). The demonstration that changing activity of V2 receptors affects the corticopapillary NaCl gradient indicates that, at least in rodents, stimulation of loop salt transport by AVP may represent an additional mechanism enhancing urine concentration.