Adrenal beta-arrestin 1 promotes physiological aldosterone production

Elevated aldosterone levels accompany and aggravate chronic heart failure (HF). Aldosterone is produced by adrenocortical zona glomerulosa (AZG) cells after angiotensin II (AngII) activation of AngII type 1 receptors (AT 1Rs), G protein coupled receptors (GPCRs) that also signal independently of G-proteins. This G protein-independent signaling, is promoted by ßarrestin (ßarr) -1 and -2, originally discovered as GPCR signaling terminators. We report here that ßarr1 promotes physiological aldosterone production in vivo, in normal rats. These findings suggest adrenal ßarr1 inhibition might be of therapeutic value for curbing HF-related hyperaldosteronism.