Effect of luminal angiotensin II and ANP on early and late cortical distal tubule HCO3- reabsorption.
Bicarbonate reabsorption was evaluated by stationary microperfusion "in vivo" early distal (ED) and late distal (LD) segments of at kidney. Intratubular pH was recorded by double-barreled of H+ exchange resin/reference (1 M KCl) microelectrodes for the determination of HCO3- reabsorption. In the presence of angiotensin II (ANG II) (10(-12) M), a significant increase in HCO3- 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 AT1-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 A1 (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 HCO3- reabsorption were observed. Our results indicate that luminal ANG II acts to stimulate Na+/H+ exchange in ED and LD segments via activation of AT1 receptors, as well as the vacuolar H(+)-adenosinetriphosphatase in LD segments. ANP does not affect HCO3- reabsorption in either ED or LD segments and does not impair the stimulation caused by ANG II.
Barreto-Chaves
M L
ML
Department of Physiology and Biophysics, University of São Paulo, Brazil.
Mello-Aires
M
M
D000042:Absorption; D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001639:Bicarbonates / Q000378:metabolism*; D001713:Biphenyl Compounds / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D007672:Kidney Cortex; D007686:Kidney Tubules, Distal / Q000187:drug effects* / Q000378:metabolism*; D019808:Losartan; D018942:Macrolides; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013777:Tetrazoles / Q000494:pharmacology
D000900:Anti-Bacterial Agents; D001639:Bicarbonates; D001713:Biphenyl Compounds; D004791:Enzyme Inhibitors; D007093:Imidazoles; D018942:Macrolides; D013777:Tetrazoles; D000804:Angiotensin II; C057360:5-(N,N-hexamethylene)amiloride; D000584:Amiloride; D009320:Atrial Natriuretic Factor; C040929:bafilomycin A1; D019808:Losartan