Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V(1) and V(2) receptors.

Peritubular arginine vasopressin (AVP) regulates bicarbonate reabsorption in the cortical distal tubule via V(1) and V(2) receptors. The dose-dependent effects of peritubular AVP on net bicarbonate reabsorption (J(HCO)) were evaluated by stationary microperfusion of in vivo early (ED; distal convoluted tubule) and late distal (LD; connecting tubule and initial collecting duct) segments of rat kidney, using double-barreled H(+)-sensitive, ion-exchange resin/reference (1 M KCl) microelectrodes. AVP (10(-11) M) perfused into peritubular capillaries increased J(HCO), compared with basal levels during intact capillary perfusion with blood, in ED and LD segments. AVP (10(-9) M) also increased J(HCO) in both segments, but the effect of AVP (10(-11) M) was significantly higher. A specificV(1)-receptor antagonist alone or with AVP (10(-11) or 10(-9) M) reduced J(HCO) below basal levels. A specific V(2)-receptor antagonist alone or plus AVP (10(-11) M) did not affect J(HCO) but increased AVP (10(-9) M)-mediated stimulation. 8-Bromoadenosine 3',5'-cyclic monophosphate alone reduced J(HCO) below basal levels and also reduced AVP (10(-11) M)-mediated stimulation. (Deamino-Cys(1), D-Arg(8)) vasopressin (a V(2)-selective agonist) also reduced J(HCO) below basal levels. These results show that peritubular AVP stimulates J(HCO) in ED and LD segments via basolateral V(1) receptors and that basolateral V(2) receptors have a dose-dependent inhibitory effect mediated by cAMP. The data also indicate that endogenous AVP stimulates distal J(HCO) via basolateral V(1) receptors.