Luminal arginine vasopressin stimulates Na+-H+ exchange and H+-ATPase in cortical distal tubule via V1 receptor

Bicarbonate reabsorption was evaluated by stationary microperfusion of in vivo early distal (ED) and late distal (LD) segments of rat kidney. Intratubular pH was recorded by double-barreled H ion-exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of luminal arginine vasopressin (AVP, 10(-9) M), a significant increase in HCO3- reabsorption was observed both in ED [from 0.931 +/- 0.061 to 2.12 +/- 0.171 nmol.cm(-2).s(-1)] and LD segments [from 0.542 +/- 0.086 to 1.67 +/- 0.111 nmol.cm(-2).s(-1)]. The addition of the V1-receptor antagonist [(d (CH2)(5), Tyr (Et)(2)) arginine vasopressin] (10(-5) M) to luminal perfusion blocked luminal AVP mediated stimulation in ED and LD segments. 5-(N, N-hexamethylene) amiloride (10(-4) M) added to luminal perfusion inhibited luminal AVP-mediated stimulation in ED (by 63.7%) and LD (by 34.1%) segments. The addition of Bafilomycin A(1) (2 x 10(-7) M) to the luminal perfusion did not affect luminal AVP-mediated stimulation in ED segments, bur reduced it (by 31.7%) in LD segments. Our results indicate that luminal AVP acts to stimulate the Na+-H+ exchange in ED and LD segments via activation of V1 receptors, as well as the vacuolar H+-ATPase in LD segments.