Modulation of the effect of arginine-vasopressin on water and ion transport in the newt early distal tubule and frog urinary bladder by V1-antagonists.

In the early distal tubule of the newt Triturus vulgaris L., 1 nM arginine-vasopressin (AVP) increased water reabsorption; the fractional reabsorption of Na+ was elevated from 46.2 +/- 6.9% to 67.8 +/- 3.9% (P < 0.001), of Cl- from 52.7 +/- 6.7% to 73.1 +/- 3.5% (P < 0.001), of Mg2+ from 48.0 +/- 7.7% to 71.7 +/- 6.3% (P < 0.001). When V1-receptors were blocked by 1 nM peptide V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl) Tyr]-[Arg8]vasopressin, 1 nM AVP increased the fractional reabsorption of fluid by 8.9% of Na+ by 10.7% and of Cl- by 11.2%, as compared with the effect of AVP alone. The fractional reabsorption of Ca2+ after addition of AVP did not differ from control; when V1-receptors were blocked in the presence of AVP, the fractional reabsorption of Ca2+ was increased by AVP. The V1-receptor block in the presence of AVP did not change the fractional reabsorption of Mg2+. Experiments on the urinary bladder of the frog Rana temporaria L. showed that 1 nM SR 49059, a non-peptide antagonist of V1a-receptors, like the peptide V1-antagonist, enhanced the AVP effect by 29%. Inhibition of protein kinase C activity by calphostin C (1 nM) mimicked the effect of V1-antagonists; the AVP hydroosmotic effect was increased by 60%. The results obtained indicate that V1-receptors modulate the effects of V2-receptor activation: their block is accompanied by an enhancement of the AVP hydroosmotic effect in the frog urinary bladder and by an increase of Na+ and Cl- reabsorption in the newt early distal tubule. The enhancement of the AVP effect owing to the V1-receptor activation seems to be mediated by a decrease in protein kinase C activity.