Deletion of the angiotensin II type 1 receptor–associated protein enhances renal sodium reabsorption and exacerbates angiotensin II–mediated hypertension

摘要: Angiotensin II type 1 receptor (AT1R)–associated protein (ATRAP) promotes AT1R internalization along with suppression of pathological activation tissue signaling. However, the functional significance ATRAP in renal sodium handling and blood pressure regulation under stimuli is not fully resolved. Here we show mice a gene-targeted disruption was comparable to that wild-type at baseline. ATRAP-knockout mice, angiotensin II–induced hypertension exacerbated extent positive balance increased by II. Renal expression sodium-proton antiporter 3, major transporter proximal tubules, urinary pH, angiotensinogen production, content unaffected. Stimulation activity epithelial channel (ENaC), distal significantly enhanced chronic infusion. The circulating aldosterone levels were comparable. response ENaC affected. Thus, deficiency II–mediated tubular This directly stimulates tubules enhances retention an aldosterone-independent manner.