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ANGPT2 — REN

Text-mined interactions from Literome

Höcherl et al., Pflugers Arch 2001 : In summary, these findings, obtained when the renin system was activated by AT1 receptor blockade, indicate that Ang II is not required to stimulate COX-2 expression and that COX-2 activity is not required to stimulate renin expression
Castrop et al., American journal of physiology. Renal physiology 2003 (Renal Artery Obstruction) : Because across-the-board data indicate that renin and cyclooxygenase-2 (COX-2) expression in the kidney cortex are regulated in parallel and because ANG II can inhibit COX-2 expression, the purpose of our study was to characterize a potential general inhibitory feedback of the renin-angiotensin system on renocortical COX-2 expression in vivo
Prieto-Carrasquero et al., Hypertension 2004 (Body Weight...) : In contrast to the inhibitory effect of Ang II on JGA renin , Ang II infusion stimulates renin protein expression in collecting ducts and maintains renin transcriptional levels in the medulla, which may contribute to the increased intrarenal Ang II levels in Ang II-dependent hypertension
Terebessy et al., Nephrol Dial Transplant 2004 : To dissect signalling mechanisms contributing to the up-regulation of the proximal renin promoter by Ang II , porcine proximal tubular cells stably expressing the rabbit AT(1) receptor ( LLC-PK/AT(1) ) were transiently transfected with a luciferase reporter construct containing the 582 bp long piece of the human renin promoter
Sadjadi et al., J Surg Res 2005 (Hypertension, Renal) : This study tested the hypothesis that an incremental increase in plasma ANG II induces the intrarenal renin-angiotensin system (RAS) in the non-ischemic kidney by an angiotensin converting enzyme (ACE) dependent mechanism
Danser et al., Hypertens Res 2010 : Renin inhibitors, similar to all renin-angiotensin system (RAS) blockers, increase the plasma concentration of renin because they attenuate the negative feedback effect of angiotensin (Ang) II on renin release ... This could potentially limit the effectiveness of renin inhibition, either because Ang II generation might occur again ( ` Ang II escape ' ), possibly even at the levels above baseline, as has been described before for angiotensin converting enzyme inhibitors, or because high levels of renin will stimulate the recently discovered ( pro ) renin receptor, and thus induce effects in an Ang independent manner
Uresin et al., Turk Kardiyol Dern Ars 2009 (Cardiovascular Diseases...) : In contrast, as the inhibition of angiotensin II (Ang II) production and effect prevents the negative feedback which helps Ang II to inhibit the renin release from the kidney, elevated Ang II levels suggest that renin enzyme, which can be considered to be the center of renin system, can be the optimal tool in the treatment
Gonzalez et al., Hypertension 2011 (Hypertension) : Collecting duct ( CD ) renin is stimulated by angiotensin (Ang) II , providing a pathway for Ang I generation and further conversion to Ang II ... In primary cultures of inner medullary CD cells, renin mRNA and ( pro ) renin protein levels increased with Ang II ( 100 nmol/L ), and candesartan ( Ang II type 1 receptor antagonist ) prevented this effect
Lindpaintner et al., Circ Res 1990 : Generation of Ang I and Ang II was inhibited in the presence of specific inhibitors of renin and converting enzyme, respectively
Köller et al., Neurosci Lett 1979 : The presence of angiotensinogen, the precursor of angiotensin II (ANG II), in brain tissue and in cerebrospinal fluid (CSF) allows stimulation of endogenous brain ANG II by renin
Antonipillai et al., Diabetes 1995 (Diabetes Mellitus, Experimental) : Similarly, ANG II ( 10 ( -8 ) mol/l ) inhibition of renin was significantly enhanced in diabetic rats ( P < 0.001 ) ... Insulin reversed the inhibitory effects of ANG II on renin in normal rats, but it blunted the effect of ANG II in diabetic rats
Nelson et al., Am J Physiol 1993 : Tonic intrarenal and/or circulating ANG II synthesis of dogs on a normal sodium diet inhibit neurogenic stimulation of renin release, since PRA responses were enhanced after blockade of ANG II
Sechi et al., Hypertension 1996 : Similarly, inhibition of Ang II generation with captopril increased plasma renin concentration and renal renin mRNA levels without altering renal or hepatic angiotensinogen mRNA or renal AT1 receptor mRNA levels
Stephan et al., Fundam Clin Pharmacol 1996 (Hypertension) : The increase in renin secretion and the induction of the converting enzyme ( ACE ) observed during treatment by ACE inhibitors ( CEIs ) could result in increased angiotensin II (ang II) synthesis when the treatment is stopped
Hollenberg et al., Hypertension 1998 : In light of the data from in vitro systems, our findings indicate that in the intact human kidney, virtually all Ang II generation is renin dependent but at least 40 % of Ang I is converted to Ang II by pathways other than ACE, presumably a chymase, although other enzyme pathways exist
Hu et al., J Hypertens 1998 : In renin- and Ang II-infused rats, respectively, plasma Ang II increased similarly from 4.5 +/- 0.8 and 4.4 +/- 0.9 to 10.8 +/- 0.7 and 10.6 +/- 0.7 pg/ml and declined similarly in the second week to 7.0 +/- 1.1 and 7.0 +/- 1.5 pg/ml. Plasma renin increased from 4.2 +/- 0.7 to 21.7 +/- 1.3 and fell from 5.9 +/- 0.5 to 0.6 +/- 0.2 ng/ml per h respectively