Effect of luminal angiotensin II and ANP on early and late cortical distal tubule HCO3- reabsorption

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+ exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO, reabsorption. In the presence of angiotensin II (ANG II) (10(-12) M), a significant increase in HCO, reabsorption was observed both in ED (from 0.930 +/- 0.060 to 2.64 +/- 0.210 nmol . cm(-2). s(-1) in luminally perfused tubules and from 0.850 +/- 0.040 to 2.03 +/- 0.210 nmol . cm(-2). s(-1) during capillary perfusion) and LD segments (from 0.310 +/- 0.130 to 2.16 +/- 0.151 nmol . cm(-2). s(-1) during luminal perfusion and from 0.530 +/- 0.031 to 2.16 +/- 0.211 nmol . cm(-2). s(-1) with capillary perfusion). The addition of the AT(1)-receptor antagonist losartan (10(-6) M) to luminal perfusion blocked luminal ANG II-mediated stimulation in ED and LD segments. 5-(N,N-hexamethylene)amiloride (10(-4) M) added to luminal perfusion inhibited luminal ANG II-mediated stimulation in ED (by 81%) and LD (by 54%) segments. The addition of bafilomycin A(1) (2 x 10(-7) M) to luminal perfusion does not affect luminal ANG II-mediated stimulation in ED segments but reduces it in LD segments (by 33%). During the addition of atrial natriuretic peptide (ANP) (10(-6) M) or ANG II plus ANP in both segments, no significant differences in HCO, reabsorption were observed. Our results indicate that luminal ANG II acts to stimulate Na+/H+ exchange in ED and LD segments via activation of AT(1) receptors, as well as the vacuolar H+-adenosinetriphosphatase in LD segments. ANP does not affect HCO, reabsorption in either ED or LD segments and does not impair the stimulation caused by ANG II.