Effects of angiotensin II on electrolyte transport in the early and late distal tubule in rat kidney

We have demonstrated in previous studies that luminal administration of low doses of angiotensin II (ANG II) stimulate and high doses of ANG II inhibit fluid and HCO3- transport in proximal tubules of rat kidney. However, the role of ANG II on Na+ and HCO3- transport in the distal nephron has not yet been fully elucidated. The superficial early and late distal tubules (DT) of the nephron segments correspond to the distal convoluted tubule and initial collecting tubule. Accordingly, we investigated the effects of ANG II on Na+, HCO3-, and K+ transport in the early and late DT by separate perfusion of these tubule segments in vivo. [H-3]inulin, Na+, K+, and total CO2 concentrations were measured in the perfusate and collected fluid, and transport of sodium (J(Na)), bicarbonate (J(HCO3)), potassium (J(K)), and fluid (J(v)) were analyzed as an index of the hormone effect. Intravenous infusion of the ANG II receptor antagonist [Sar(1),Ile(8)]ANG II (1 mu g . kg(-1). min(-1)) decreased J(v), J(Na), and J(HCO3) in the early DT and decreased J(v) and J(Na) in the late DT. Addition of ANG II (10(-11) M) to the tubular perfusate significantly increased the J(v), J(Na), and J(HCO3) in the early DT. Similar studies in late DT demonstrated an increase in J(v) and J(Na), decrease in J(K), but no effect on J(HCO3) The effects of ANG II on fluid and ion transport were abolished by the luminal application of amiloride (10(-3) M) and of the angiotensin-receptor blocker [Sar1,Ile(8)]ANG II (10(-6) M). These results suggest that ANG II stimulates Na+/H+ exchange in the early DT (distal convoluted tubule) and amiloride-sensitive Na+ transport (Na+ channels) in the late DT (initial collecting tubule) of cortical nephrons.