STIMULATION OF RAT RENAL MEDULLARY NA+/K+-ATPASE BY ARGININE VASOPRESSIN IS MEDIATED BY THE V2 RECEPTOR

In previous studies, we have demonstrated that 1-10 fmol arginine vasopressin (AVP)/l maximally stimulates the activity of the enzyme Na+/K+-ATPase in the rat renal medullary thick ascending limb (MTAL) of Henle's loop after 4 or 10 min of stimulation when measured using a cytochemical bioassay. We have tested the hypothesis that this stimulation is mediated by the V2 receptor in the MTAL. A cytochemical bioassay was used to investigate the effect of specific V1 and V2/V1 antagonists and a synthetic V2 agonist [1-deamino,8-D-arginine]-vasopressin (dDAVP), on the activity of Na+/K+-ATPase. There was no effect of the V1 antagonist (1 fmol-1 μmol/l) in inhibiting the activity of Na+/K+-ATPase stimulated by 1 fmol AVP/l. In contrast, 100 pmol of the V2/V1 antagonist/l significantly (P < 0.001) inhibited the stimulation of Na+/K+-ATPase activity by 1 fmol AVP/l from 55.5 ± 4.3 (S.E.M.) to 31.9 ± 1.6 mean integrated extinction (MIE) after 4 min of stimulation and from 67.0 ± 3.2 to 36.9 ± 0.7 MIE after 10 min of stimulation. Similarly, the stimulation of Na+/K+-ATPase by 10 fmol dDAVP/l was inhibited by the V2/V1 antagonist from 55.1 ± 1.0 to 26.1 ± 0.5 MIE after 4 min of stimulation. We conclude that the stimulation of Na+/K+-ATPase by AVP is mediated by the V2 receptor in the rat renal MTAL.