An electrophysiological study of angiotensin II regulation of Na-HCO3 cotransport and K conductance in renal proximal tubules

In the first part of our study, we described the effect of picomolar concentrations of angiotensin II (AII) on cell membrane potential (Vb) and cell pH (pHi) of isolated perfused rabbit renal proximal tubules. In the present publication we summarize respective observations with micromolar concentrations of AII. With a few exceptions nearly all experiments showed mirror-image-like results. In the majority of the experiments 10(-6) mol/l AII, when applied from the bath (but not when applied from the lumen), slightly hyperpolarized the cells by -3.4 +/- 0.3 mV (mean +/- SEM, n = 20) and alkalinized them by up to 0.06 pH units, while the lower AII concentrations, which were applied in the previous study, depolarized and acidified. The present observations suggest that micromolar concentrations of AII inhibit basolateral Na-HCO3 cotransport. This conclusion was confirmed by a decreasing Vb response to step changes of basolateral HCO3 concentration. In addition, there was a tendency of the Vb response to K concentration steps to decrease, but measurements of the voltage divider ratio did not point to a significant inhibition of a basolateral K conductance. In spite of the almost perfect reciprocity of the results with 10(-6) and 10(-11) mol/l AII, some specific observations suggest that micromolar concentrations of AII do not simply cause mirror-image-like effects, but influence still further transport systems compared to picomolar concentrations.