Effects of angiotensin II on the CO2dependence of HCO3−reabsorption by the rabbit S2 renal proximal tubule

Abstract

Previous authors showed that, at low doses, both basolateral and luminal ANG II increase the proximal tubule's HCO3−reabsorption rate ( JHCO3). Using out-of-equilibrium CO2/HCO3−solutions, we demonstrated that basolateral CO2increases JHCO3. Here, we examine interactions between ANG II and CO2in isolated, perfused rabbit S2 segments. We first used equilibrated 5% CO2/22 mM HCO3−/pH 7.40 in bath and lumen. At 10−11M, basolateral (BL) ANG II increased JHCO3by 41%, and luminal ANG II increased JHCO3by 35%. At 10−9M, basolateral ANG II decreased JHCO3by 43%, whereas luminal ANG II was without effect. Second, we varied [CO2]BLfrom 0 to 20% at fixed [HCO3−]BLand pHBL. Fractional stimulation produced by BL 10−11M ANG II falls when [CO2]BLexceeds 5%. Fractional inhibition produced by BL 10−9M ANG II tends to rise when [CO2]BLexceeds 5%. Regarding luminal ANG II, fractional stimulation produced by 10−11M ANG II fell monotonically as [CO2]BLrose from 0 to 20%. Fractional inhibition produced by 10−9M ANG II rose monotonically with increasing [CO2]BL. Viewed differently, ANG II at 10−11M tended to reduce stimulation by CO2, and at 10−9M, produced an even greater reduction. In conclusion, the mutual effects of 1) ANG II on the JHCO3response to basolateral CO2and 2) basolateral CO2on the JHCO3responses to ANG II suggest that the signal-transduction pathways for ANG II and basolateral CO2intersect or merge.