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Query: UMLS:C0004135 (ATM)
 13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When angiotensin II or AT1 receptor is experimentally inhibited during the perinatal period, either by pharmacological intervention or genetic manipulation, the kidney develops with profound structural abnormalities. Most prominent are hypertrophy of arterial vasculatures and atrophy of the papilla. Although the mechanism by which the vascular hypertrophy occurs remains unknown, study of the atrophic papilla gives us a new clue for understanding the physiological role of angiotensin. Mutant mice completely devoid of AT1 receptor fail to develop the renal pelvis and the ureteral peristaltic movement. Normally, angiotensin and AT1 receptor are transiently up-regulated around the renal outlet at birth. Thus angiotensin II induces the peristaltic machinery during the perinatal period in a timely fashion to accommodate the dramatic increase in urine production that occurs during the transition from intra- to extra-uterine life. Further studies revealed that in adult animals angiotensin augments the peristaltic movement when the urinary tract is partially obstructed, thereby protecting the kidney from hydronephrosis. This newly discovered function of angiotensin to protect kidney architecture at the time of urine outflow obstruction is reminiscent of its similar kidney structure-protecting function that is active during arterial blood flow obstruction.
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PMID:The renin angiotensin system and kidney development. 1182 79

The renin-angiotensin system (RAS) plays a critical role in kidney development. Mutations in the genes encoding components of the RAS or pharmacological inhibition of RAS in mice or humans cause a spectrum of congenital abnormalities of the kidney and urinary tract (CAKUT). The observed defects include renal vascular abnormalities, abnormal glomerulogenesis, renal papillary hypoplasia, hydronephrosis, aberrant ureteric bud (UB) budding, duplicated collecting system and renal tubular dysgenesis. Little is known about the potential role of Ang II and its receptors in the morphogenesis of the UB and renal collecting system. This review emphasizes a novel role for the RAS in the development of the UB, collecting ducts and renal medulla. We observe that UB and surrounding stroma express angiotensinogen and Ang II AT1 receptors (AT1R) in vivo. Ang II stimulates UB cell branching in collagen gel cultures in vitro and induces UB morphogenesis in intact whole embryonic metanephroi grown ex vivo. In contrast, treatment of metanephroi with the AT1R antagonist candesartan inhibits UB branching. In addition, Ang II induces tyrosine phosphorylation of the epidermal growth factor receptor (EGFR) in UB cells. Furthermore, Ang II-stimulated UB morphogenesis is abrogated by inhibition of EGFR tyrosine kinase activity. In summary: 1) Ang II, acting via the AT1R, stimulates UB branching; 2) This process depends on tyrosine phosphorylation of the EGFR. Together, these data indicate that cooperation of AT1R and EGFR signaling performs essential functions during renal collecting system development via control of UB branching morphogenesis.
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PMID:A new role for the renin-angiotensin system in the development of the ureteric bud and renal collecting system. 1911 May 30