An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model.

摘要: Angiotensin II type 1 receptor-associated protein (ATRAP) promotes AT1R internalization along with suppression of hyperactivation tissue signaling. Here, we provide evidence that renal ATRAP plays a critical role in suppressing hypertension mouse remnant kidney model chronic disease. The effect 5/6 nephrectomy on endogenous expression was examined the C57BL/6 and 129/Sv mice. While mice showed decreased developed hypertension, exhibited increased resistance to progressive hypertension. Consequently, hypothesized downregulation is involved pathogenesis Interestingly, ATRAP-knockout hypertension-resistant background caused plasma volume. Moreover, knockout compared wild-type after nephrectomy, epithelial sodium channel α-subunit tumor necrosis factor-α significantly enhanced, concomitant membrane angiotensin receptor kidneys. Thus, onset progression of blood pressure elevation by mass reduction, and implicates as therapeutic target for hypertension