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10.1161/HYPERTENSIONAHA.107.107268 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.107.107268 18413493!2398652!18413493     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2008 ; 51 (6): 1597-604 Nephropedia Template TP {{tp|p=18413493|t=2008. The collecting duct is the major source of prorenin in diabetes |pdf=|usr=}}{{18413493}} gab.com Text The collecting duct is the major source of prorenin in diabetes JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=18413493 #FOAvip In addition to the juxtaglomerular apparatus, renin is also synthesized in renal tubular epithelium, including the collecting duct (CD). Angiotensin (Ang) II differentially regulates the synthesis of juxtaglomerular (inhibition) and CD (stimulation) renin. Because diabetes mellitus, a disease with high intrarenal renin-Ang system and Ang II activity, is characterized by high prorenin levels, we hypothesized that the CD is the major source of prorenin in diabetes. Renin granular content was visualized using in vivo multiphoton microscopy of the kidney in diabetic Munich-Wistar rats. Diabetes caused a 3.5-fold increase in CD renin, in contrast to less pronounced juxtaglomerular changes. Ang II type 1 receptor blockade with Olmesartan reduced CD renin to control levels but significantly increased juxtaglomerular renin. Using a fluorogenic renin assay, the prorenin component of CD renin content was measured by assessing the difference in enzymatic activity of medullary homogenates before and after trypsin activation of prorenin. Trypsinization caused no change in control renin activity but a 5-fold increase in diabetes. Studies on a CD cell line (M1) showed a 22-fold increase in renin activity after trypsinization and a further 35-fold increase with Ang II treatment. Therefore, prorenin significantly contributes to baseline CD renin. Diabetes, possibly via Ang II, greatly stimulates CD prorenin and causes hyperplasia of renin-producing connecting segments. These novel findings suggest that, in a rat model of diabetes, prorenin content and release from the CD may be more important than the juxtaglomerular apparatus in contrast to the existing paradigm. Twit Text FOAVip The collecting duct is the major source of prorenin in diabetes ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=18413493 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18413493 #FOAvip English Wikipedia <ref>{{Cite pmid|18413493}}</ref> The collecting duct is the major source of prorenin in diabetes #MMPMID18413493 Kang JJ; Toma I; Sipos A; Meer EJ; Vargas SL; Peti-Peterdi J Hypertension 2008[Jun]; 51 (6): 1597-604 PMID18413493show ga In addition to the juxtaglomerular apparatus, renin is also synthesized in renal tubular epithelium, including the collecting duct (CD). Angiotensin (Ang) II differentially regulates the synthesis of juxtaglomerular (inhibition) and CD (stimulation) renin. Because diabetes mellitus, a disease with high intrarenal renin-Ang system and Ang II activity, is characterized by high prorenin levels, we hypothesized that the CD is the major source of prorenin in diabetes. Renin granular content was visualized using in vivo multiphoton microscopy of the kidney in diabetic Munich-Wistar rats. Diabetes caused a 3.5-fold increase in CD renin, in contrast to less pronounced juxtaglomerular changes. Ang II type 1 receptor blockade with Olmesartan reduced CD renin to control levels but significantly increased juxtaglomerular renin. Using a fluorogenic renin assay, the prorenin component of CD renin content was measured by assessing the difference in enzymatic activity of medullary homogenates before and after trypsin activation of prorenin. Trypsinization caused no change in control renin activity but a 5-fold increase in diabetes. Studies on a CD cell line (M1) showed a 22-fold increase in renin activity after trypsinization and a further 35-fold increase with Ang II treatment. Therefore, prorenin significantly contributes to baseline CD renin. Diabetes, possibly via Ang II, greatly stimulates CD prorenin and causes hyperplasia of renin-producing connecting segments. These novel findings suggest that, in a rat model of diabetes, prorenin content and release from the CD may be more important than the juxtaglomerular apparatus in contrast to the existing paradigm. |Angiotensin II Type 1 Receptor Blockers/pharmacology[MESH] |Angiotensin II/metabolism/pharmacology[MESH] |Animals[MESH] |Cell Division/physiology[MESH] |Cells, Cultured[MESH] |Diabetes Mellitus, Experimental/metabolism[MESH] |Diabetic Nephropathies/*metabolism[MESH] |Disease Models, Animal[MESH] |Hypertension, Renal/*metabolism[MESH] |Imidazoles/pharmacology[MESH] |Immunohistochemistry[MESH] |Juxtaglomerular Apparatus/cytology/*metabolism[MESH] |Kidney Tubules, Collecting/cytology/*metabolism[MESH] |Microscopy, Fluorescence[MESH] |Quinacrine[MESH] |Rats[MESH] |Rats, Wistar[MESH] |Renin/*metabolism[MESH] |Tetrazoles/pharmacology[MESH] |Trypsin[MESH]The collecting duct is the major source of prorenin in diabetes (epmc).pdf DeepDyve Pubget Overpricing