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Effects of angiotensin II on the CO₂ dependence of HCO₃^– reabsorption by the rabbit S2 renal proximal tubule

Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut

Submitted 12 July 2005 ; accepted in final form 26 September 2005

Previous authors showed that, at low doses, both basolateral and luminal ANG II increase the proximal tubule's HCO₃^– reabsorption rate (J_HCO3). Using out-of-equilibrium CO₂/HCO₃^– solutions, we demonstrated that basolateral CO₂ increases J_HCO3. Here, we examine interactions between ANG II and CO₂ in isolated, perfused rabbit S2 segments. We first used equilibrated 5% CO₂/22 mM HCO₃^–/pH 7.40 in bath and lumen. At 10^–11 M, basolateral (BL) ANG II increased J_HCO3 by 41%, and luminal ANG II increased J_HCO3 by 35%. At 10^–9 M, basolateral ANG II decreased J_HCO3 by 43%, whereas luminal ANG II was without effect. Second, we varied [CO₂]_BL from 0 to 20% at fixed [HCO₃^–]_BL and pH_BL. Fractional stimulation produced by BL 10^–11 M ANG II falls when [CO₂]_BL exceeds 5%. Fractional inhibition produced by BL 10^–9 M ANG II tends to rise when [CO₂]_BL exceeds 5%. Regarding luminal ANG II, fractional stimulation produced by 10^–11 M ANG II fell monotonically as [CO₂]_BL rose from 0 to 20%. Fractional inhibition produced by 10^–9 M ANG II rose monotonically with increasing [CO₂]_BL. Viewed differently, ANG II at 10^–11 M tended to reduce stimulation by CO₂, and at 10^–9 M, produced an even greater reduction. In conclusion, the mutual effects of 1) ANG II on the J_HCO3 response to basolateral CO₂ and 2) basolateral CO₂ on the J_HCO3 responses to ANG II suggest that the signal-transduction pathways for ANG II and basolateral CO₂ intersect or merge.

kidney; out-of-equilibrium solutions; acid-base; volume reabsorption

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