V(1) receptors in luminal action of vasopressin on distal K(+) secretion.

Luminal perfusion with collected proximal fluid increases distal K(+) secretion compared with artificial solutions. Arginine vasopressin (AVP), present in luminal fluid, might be responsible for this observation. K(+) secretion rate (J(K)) was measured by K(+)-sensitive microelectrodes during paired luminal stationary microperfusion with control and AVP-containing 0.5 mM K(+) solutions. J(K) was 1.34 +/- 0.35 (n = 24 tubules) nmol x cm(-2) x s(-1) during perfusion with 10(-9) M AVP, against 0.90+/-0.12 nmol x cm(-2) x s(-1) (n = 21) in control (P<0.02). With 10(-9) M AVP+10(-6) M beta-mercapto-beta-beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2)-Arg(8) vasopressin (MCMV), a specific peptide V(1)-receptor antagonist, J(K) was 0.36+/-0.067 against 0.77+/-0.10 (control; n = 9) nmol x cm(-2) x s(-1) (P<0.01). With 10(-6) M MCMV alone, J(K) was 0.37+/-0.04 against a control of 0.62+/-0.06 (n = 19) nmol. cm(-2). s(-1) (P<0.01). A peptide V(2) antagonist had no such effect. In Brattleboro rats, which do not produce endogenous AVP, MCMV had no effect when given alone, although AVP still stimulated J(K). In conclusion, luminal AVP stimulates distal J(K) significantly. The V(1) antagonist MCMV inhibits the effect of AVP but also reduces J(K) when given alone. This suggests that AVP acts luminally via V(1) receptors but also that there appears to be a background effect of endogenous AVP blocked by the antagonist.