Autoantibodies against angiotensin and adrenergic receptors: more than a biomarker?

摘要

Agonistic autoantibodies (AAs) directed against receptors of the sympathetic nervous system and the reninangiotensin system have been suggested to contribute to cardiovascular and renal disease, in particular hypertension, preeclampsia, and graft failure in kidney transplantation patients. Consequently, they are now also being studied as biomarker for these conditions. This commentary summarizes our current understanding of these AAs, critically discussing whether they truly act as agonist, and focusing on the wide array of assays that are currently used for their quantification. Multiple studies have been reported on the existence of agonistic autoantibodies (AAs) directed against receptors of the sympathetic nervous system (?-adrenoceptors, ?R) and the reninangiotensin system (angiotensin II type 1 receptor, AT1R). Obviously, if acting as agonists, such antibodies might contribute to cardiovascular disease. Indeed, ?R-AAs and AT1R-AAs were initially detected based on their ability to activate their receptor in cultured neonatal rat cardiomyocytes, resulting in an increase in beating rate [1,2]. The fact that the ?R antagonist prazosin and the AT1R antagonist losartan respectively, blocked this effect, confirmed their agonistic capacity [1,2].