AT1AA (Angiotensin II type-1 receptor autoantibodies) were first detected in patients with primary aldosteronism (PA) because of aldosterone-producing adenoma (APA) with an in-house developed assay, but it remained unclear if they can be ascertained also with commercially available assays and if they have a functional role. Aims of our study were to investigate if (1) commercially available kits allow detection of raised AT1AA titer in APA; (2) this titer is normalized by adrenalectomy; and (3) AT1AA display any biological roles in vitro. We measured with 2 ELISA kits the AT1AA titer in serum of APA patients and its changes after adrenalectomy. We also investigated AT1AA bioactivity by using AT1-R (angiotensin type-1 receptor)–transfected Chinese hamster ovary and human adrenocortical carcinoma cells, and by measuring aldosterone synthase ( CYP11B2 ) expression in human adrenocortical carcinoma cells after incubation with IgG. Both kits allowed detection of higher AT1AA levels in APA patients than in healthy subjects; surgical cure of PA did not decrease this titer at 1-month follow-up. Human adrenocortical carcinoma cells stimulation with IgG purified from sera of APA patients increased both CYP11B2 expression and aldosterone release (+40% and +76%, respectively, versus healthy subjects). However, no detectable effect of IgG was seen in Chinese hamster ovary cells expressing AT1-R. These findings support the contentions that (1) the raised AT1AA titer does not seem to be a consequence of hyperaldosteronism as it did not normalize after its cure; (2) AT1AA act as weak stimulators of aldosterone biosynthesis, but this effect can be identified only by using a sensitive in vitro technique.
