The effects of angiotensin II (All) on proximal tubular reabsorption have been evaluated in 6 healthy volunteers under normal salt and water balance. One-hour clearance periods were performed before, during and after the infusion of pressor doses of All; in 3 of the 6 subjects, the study was repeated with lower doses of All. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were determined by the clearances of inulin and PAH, and the fractional excretion of lithium (FELi) was considered as an index of proximal sodium reabsorption. The effects of AH on the fractional excretion of β₂ microglobulin (FEβ₂M) were also studied. Both doses of All decreased GFR and RPF and increased the filtration fraction (FF); the modifications of these parameters, as well as the reduction of FELi and the fractional excretion of sodium (FENa) and the increase of plasma aldosterone and of plasma atrial natriuretic peptide (ANP), were more evident with pressor doses of All, which increased the blood pressure from 129/83 to 142/95 mm Hg (p < 0.01). All did not modify FEβ₂M in either study. During All, FELi decreased less than FENa and both were closely and inversely related to the variations of FF, whilst no relationship was present between FEβ₂M and FF. These results suggest that, in normal humans, the All-induced rise of FF may be an important factor, even if not the only one, in enhancing the proximal reabsorption of lithium and thus of sodium, whilst it does not affect the absorption of β₂M.

To verify if exogenous prostaglandin E₂ (PGE₂) is able to release antidiuretic hormone (ADH) and if endogenous angiotensin II plays a role in this eventual PGE₂-induced stimulation of vasopressin, increasing doses of PGE₂ were infused in 6 normal volunteers before (PGE₂ study) and after the administration of 100 mg of captopril (captopril study). PGE₂, even at an infusion rate of 40 and 60 ng/kg/min, did not modify blood pressure when it was infused alone; a significant fall of blood pressure was observed, in contrast, in the captopril study. PGE₂ alone doubled the plasma levels of ADH. One hour after the subjects had been pre-treated with captopril, plasma levels of ADH fell by about 38%, then they increased by about 60% during the infusion of PGE₂. These results suggest that in normal man endogenous angiotensin II is an important non-osmotic regulator of plasma ADH and that exogenous PGE₂ can stimulate maximally the release of ADH only when the renin-angiotensin system is not impaired.