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 CO2 increases JHCO3. 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 JHCO3 by 41%, and luminal ANG II increased JHCO3 by 35%. At 10−9 M, basolateral ANG II decreased JHCO3 by 43%, whereas luminal ANG II was without effect. Second, we varied [CO2]BL from 0 to 20% at fixed [HCO3−]BL and pHBL. 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 JHCO3 response to basolateral CO2 and 2) basolateral CO2 on the JHCO3 responses to ANG II suggest that the signal-transduction pathways for ANG II and basolateral CO2 intersect or merge.
Angiotensin II (AngII) induces the expression of suppressor of cytokine signaling (SOCS)-3 in rat hypothalamus - a mechanism for desensitization of AngII signaling