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10.1002/psp4.12177 http://scihub22266oqcxt.onion/10.1002/psp4.12177 C5488119!5488119!28556624     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       CPT+Pharmacometrics+Syst+Pharmacol 2017 ; 6 (6): 393-400 Nephropedia Template TP {{tp|p=28556624|t=2017. A Quantitative Systems Physiology Model of Renal Function and Blood Pressure Regulation: Application in Salt?Sensitive Hypertension |pdf=|usr=}}{{28556624}} gab.com Text A Quantitative Systems Physiology Model of Renal Function and Blood Pressure Regulation: Application in Salt Sensitive Hypertension JO: CPT Pharmacometrics Syst Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28556624 #FOAvip Salt?sensitivity (SS) refers to changes in blood pressure in response to changes in sodium intake. SS individuals are at greater risk for developing kidney disease, and also respond differently to antihypertensive therapies compared to salt?resistant (SR) individuals. In this study we used a systems pharmacology model of renal function (presented in a companion article) to evaluate the ability of proposed mechanisms to produce salt?sensitivity. The model reproduced previously published data on renal functional changes in response to salt?intake, and also predicted that glomerular pressure, a variable that is not easily evaluated clinically but is a key factor in renal injury, increases with salt intake in SS hypertension. We then used the model to generate mechanistic insight into the differential blood pressure and glomerular pressure responses to angiotensin converting enzyme (ACE) inhibitors, thiazide diuretics, and calcium channel blockers observed in SS and SR hypertension. Twit Text FOAVip A Quantitative Systems Physiology Model of Renal Function and Blood Pressure Regulation: Application in Salt Sensitive Hypertension ????CPT Pharmacometrics Syst Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28556624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28556624 #FOAvip English Wikipedia <ref>{{Cite pmid|28556624}}</ref> A Quantitative Systems Physiology Model of Renal Function and Blood Pressure Regulation: Application in Salt?Sensitive Hypertension #MMPMID28556624 Hallow K; Gebremichael Y CPT Pharmacometrics Syst Pharmacol 2017[Jun]; 6 (6): 393-400 PMID28556624show ga Salt?sensitivity (SS) refers to changes in blood pressure in response to changes in sodium intake. SS individuals are at greater risk for developing kidney disease, and also respond differently to antihypertensive therapies compared to salt?resistant (SR) individuals. In this study we used a systems pharmacology model of renal function (presented in a companion article) to evaluate the ability of proposed mechanisms to produce salt?sensitivity. The model reproduced previously published data on renal functional changes in response to salt?intake, and also predicted that glomerular pressure, a variable that is not easily evaluated clinically but is a key factor in renal injury, increases with salt intake in SS hypertension. We then used the model to generate mechanistic insight into the differential blood pressure and glomerular pressure responses to angiotensin converting enzyme (ACE) inhibitors, thiazide diuretics, and calcium channel blockers observed in SS and SR hypertension. äA Quantitative Systems Physiology Model of Renal Function and Blood Pr(epmc).pdf DeepDyve Pubget Overpricing