2001
DOI: 10.1016/s0090-4295(01)01156-6
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Partial ureteral obstruction dysregulates the renal renin-angiotensin system in the fetal sheep kidney

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Cited by 22 publications
(15 citation statements)
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“…Ureteral obstruction causes renin secretion to rise (21,27,28) (14). Ishidoya et al showed the importance that the RAS has for renal fibrosis, using an Ang II receptor antagonist and an ACE inhibitor for its suppression (18 Kagami et al (20), and Pimentel et al (29) reported that the elevated TGF-b seen in obstruction is mediated by Ang II.…”
Section: Discussionmentioning
confidence: 99%
“…Ureteral obstruction causes renin secretion to rise (21,27,28) (14). Ishidoya et al showed the importance that the RAS has for renal fibrosis, using an Ang II receptor antagonist and an ACE inhibitor for its suppression (18 Kagami et al (20), and Pimentel et al (29) reported that the elevated TGF-b seen in obstruction is mediated by Ang II.…”
Section: Discussionmentioning
confidence: 99%
“…Under basal conditions, renin produced by juxtaglomerular cells is sufficient to main BP and intravascular volume (71). Upon prolonged threat to volume homeostasis (i.e., through exposing mice to a low salt diet and ACE inhibitors) additional cells along afferent arterioles express renin, in angiotensinogen-deficient mice renin is even expressed by fibroblasts (pericytes) all through the kidney cortex (80,81). Models of CKD are also associated with recruitment of additional renin-producing cells.…”
Section: Reninmentioning
confidence: 99%
“…Functionally, AT2 receptors are believed to mediate programmed cell death (Yamada et al 1996), while AT1 receptor activation has been linked to proliferative/hypertrophic responses. It should not be surprising that the renin-angiotensin system also plays a direct role in the anomalous development of the upper urinary tract in the setting of ureteral obstruction (Ayan et al 2001).…”
Section: Local Renin-angiotensin Systemsmentioning
confidence: 99%
“…Obstruction of the bladder outlet and the ureter in the fetal sheep has been linked to upregulation of the renal RAS, with elevated levels of renin, angiotensinogen, and AT1 receptor mRNA (Ayan et al 2001). In addition, downstream effectors were also increased, including TGF-ß, PDGF, and HBEGF (Park et al 1998), as well as in tissue inhibitors of metalloproteinases (Peters et al 1992b;Gobet et al 1999).…”
Section: Local Renin-angiotensin Systemsmentioning
confidence: 99%