Atrial natriuretic peptide levels during angiotensin infusion and indomethacin administration are consistent with angiotensin-mediated regulation in man.

Low-dose angiotensin II (ANG II) infusion raised plasma atrial natriuretic peptide (ANP) levels only when endogenous renin-angiotensin levels were low, as in aldosterone-producing adenoma. When plasma renin activity (PRA) levels rose tenfold following removal of the tumour, low-dose ANG II infusion no longer stimulated ANP, but fivefold higher doses did. Indomethacin lowered both PRA and ANP in Bartter's syndrome and in normal subjects. The effect of indomethacin on ANP is probably not direct, since it did not lower ANP in aldosterone-producing adenoma. Neither did it lower PRA in aldosterone-producing adenoma, and in most studies ANP and PRA moved in parallel, consistent with positive regulation of ANP by ANG II. When ANG II infusion stimulated ANP, it also raised blood pressure, which could therefore be mediating the effects of ANG II on ANP. However, both PRA and ANP are high in Bartter's syndrome, while blood pressure is normal or low, and indomethacin lowers PRA and ANP in Bartter's syndrome and in normal subjects without lowering the blood pressure. The relative importance of regulatory factors such as central blood volume/atrial pressure and ANG II level probably varies in different situations. In aldosterone-producing adenoma, a high central blood volume appears to over-ride the effect of a low ANG II level. In Bartter's syndrome a high ANG II level appears to over-ride the effect of low central blood volume.