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 newtTriturus 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-(-mercapto-,-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 frogRana temporaria L. showed that 1 nM SR 49059, a non-peptide antagonist of V_1a-receptors, like the peptide V₁antagonist, 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.