Angiotensin II directly stimulates sodium transport in rabbit proximal convoluted tubules

Numerous previous studies have proposed a role for angiotensin II (AII) in the renal regulation of salt balance. At least one nephron site, the proximal convoluted segment, has been implicated in this role. We used in vitro microperfusion of rabbit proximal convoluted tubules to further examine this question. To insure use of appropriate in vivo concentrations as well as potency of the hormone in vitro, we measured plasma AII levels by radioimmunoassay in normal, sodium-depleted, and adrenalectomized rabbits, and measured AII activity by bioassay after incubation in various microperfusion baths. Plasma levels ranged from ~2 x 10^-11 to 5 x 10^-11 M. AII activity was stable in Ringer's solution plus albumin, but not in rabbit serum or Ringer's solution plus fetal calf serum. In Ringer's solution plus albumin, physiologic concentrations of AII stimulated volume reabsorption (J(v)). 10^-11 M AII increased J(v) by 16% (P < 0.01). 10^-10 M AII produced a lesser increase, 7.5% (P < 0.05). At a frequently studied, but probably pharmacologic dose, 10^-7 M AII inhibited J(v) by 24% (P < 0.001). AII at 10^-11 M did not stimulate J(v) in the presence of 10^-7 M saralasin. Though previous studies have suggested agonistic effects of saralasin alone in epithelia, we found no significant effect of 10^-7 M saralasin on J(v). None of the AII doses measurably changed transepithelial voltage. We conclude that AII in physiologic doses directly stimulates J(v) in proximal convoluted tubules and this effect is probably receptor mediated and, within the limits of detection, electroneutral.