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10.1111/j.1582-4934.2009.00778.x http://scihub22266oqcxt.onion/10.1111/j.1582-4934.2009.00778.x C3828848!3828848!19432815     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2010 ; 14 (6a): 1318-27 Nephropedia Template TP {{tp|p=19432815|t=2010. The renin?angiotensin system as a primary cause of polyarteritis nodosa in rats |pdf=|usr=}}{{19432815}} gab.com Text The renin angiotensin system as a primary cause of polyarteritis nodosa in rats JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19432815 #FOAvip Polyarteritis nodosa is a necrotizing vasculitis of medium-sized arteries of unknown origin. Hypertension is present in 30% of patients with polyarteritis nodosa. In those cases, high renin levels are thought to be secondary to renal involvement. The present study was performed to identify causal factors of polyarteritis nodosa. In cyp1a1ren-2 transgenic rats, vasculitis of medium-sized arteries resembling classical polyarteritis nodosa can be induced. In this model, oral administration of indole-3-carbinol (I3C) activates the liver-specific cyp1a1 promoter, leading to prorenin expression in a dose-dependent manner. After the first 6 weeks of chronic induction with 0.125% I3C, the mean arterial pressure reached a plateau of about 170 mmHg. Ten out of 11 I3C-treated rats, which were chronically instrumented with a telemetric device to measure blood pressure, developed polyarteritis nodosa within 10 weeks of I3C treatment. I3C alone or instrumentation alone did not cause polyarteritis nodosa. The angiotensin-converting enzyme inhibitor captopril completely prevented the development of polyarteritis nodosa, indicating that local angiotensin II generation is a pathogenetic factor in this model. The renin?angiotensin system can play a primary role in the development of polyarteritis nodosa in rats. Twit Text FOAVip The renin angiotensin system as a primary cause of polyarteritis nodosa in rats ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19432815 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19432815 #FOAvip English Wikipedia <ref>{{Cite pmid|19432815}}</ref> The renin?angiotensin system as a primary cause of polyarteritis nodosa in rats #MMPMID19432815 Peters BS; Kuttler B; Beineke A; Lorenz G; Thiele A; Nicolai O; Rettig R; Mullins JJ; Peters J J Cell Mol Med 2010[Jun]; 14 (6a): 1318-27 PMID19432815show ga Polyarteritis nodosa is a necrotizing vasculitis of medium-sized arteries of unknown origin. Hypertension is present in 30% of patients with polyarteritis nodosa. In those cases, high renin levels are thought to be secondary to renal involvement. The present study was performed to identify causal factors of polyarteritis nodosa. In cyp1a1ren-2 transgenic rats, vasculitis of medium-sized arteries resembling classical polyarteritis nodosa can be induced. In this model, oral administration of indole-3-carbinol (I3C) activates the liver-specific cyp1a1 promoter, leading to prorenin expression in a dose-dependent manner. After the first 6 weeks of chronic induction with 0.125% I3C, the mean arterial pressure reached a plateau of about 170 mmHg. Ten out of 11 I3C-treated rats, which were chronically instrumented with a telemetric device to measure blood pressure, developed polyarteritis nodosa within 10 weeks of I3C treatment. I3C alone or instrumentation alone did not cause polyarteritis nodosa. The angiotensin-converting enzyme inhibitor captopril completely prevented the development of polyarteritis nodosa, indicating that local angiotensin II generation is a pathogenetic factor in this model. The renin?angiotensin system can play a primary role in the development of polyarteritis nodosa in rats. äThe renin?angiotensin system as a primary cause of polyarteritis nodos(epmc).pdf DeepDyve Pubget Overpricing