The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal convoluted tubule (PCT) volume absorption and bicarbonate transport. Neither 10(-11) M, 10(-10) M, nor 2 x 10(-8) M luminal angiotensin II significantly affected PCT transport. When tubules were first perfused with enalaprilat to inhibit endogenous angiotensin II production, addition of 10(-10) M luminal angiotensin II increased volume absorption (0.72 +/- 0.08 vs. 0.86 +/- 0.07 nl x mm(-1) xmin(-1), P < 0.01) and bicarbonate transport (52.3 +/- 3.7 vs. 67.9 +/- 4.2 pmol x mm(-1) min(-1), P < 0.01). Addition of 10(-6) M losartan, an AT1 inhibitor, to the luminal perfusate inhibited volume absorption (0.95 +/- 0.14 vs. 0.72 +/- 0.11 nl x mm(-1) x min(-1), P < 0.05) and bicarbonate transport (65.0 +/- 7.3 vs. 54.7 +/- 9.2 pmol x mm(-1) x min(-1), P < 0.05). Addition of 10(-4) M luminal PD-123319, an AT2 inhibitor, was without effect. In tubules perfused with 10(-4) M luminal enalaprilat and 10(-4) M luminal PD-123319, addition of 10(-10) M luminal angiotensin II in the experimental period resulted in a stimulation in volume absorption (0.61 +/- 0.08 vs. 0.81 +/- 0.10 nl x mm(-1) x min(-1), P < 0.01) and bicarbonate transport (49.9 +/- 6.3 vs. 77.4 +/- 14.3 pmol x mm(-1) x min(-1), P < 0.01). In tubules perfused with 10(-6) M losartan and 10(-4) M enalaprilat, addition of luminal 10(-10) M angiotensin II resulted in no change in transport. These data are consistent with endogenous angiotensin II affecting PCT bicarbonate transport in vitro via luminal AT1 receptors.