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10.1152/ajprenal.00294.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00294.2016 27707706!5210208!27707706     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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 311 (6): F1217-F1229 Nephropedia Template TP {{tp|p=27707706|t=2016. Solute transport and oxygen consumption along the nephrons: effects of Na+ transport inhibitors |pdf=|usr=}}{{27707706}} gab.com Text Solute transport and oxygen consumption along the nephrons: effects of Na+ transport inhibitors JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27707706 #FOAvip Sodium and its associated anions are the major determinant of extracellular fluid volume, and the reabsorption of Na(+) by the kidney plays a crucial role in long-term blood pressure control. The goal of this study was to investigate the extent to which inhibitors of transepithelial Na(+) transport (T(Na)) along the nephron alter urinary solute excretion and T(Na) efficiency and how those effects may vary along different nephron segments. To accomplish that goal, we used the multinephron model developed in the companion study (28). That model represents detailed transcellular and paracellular transport processes along the nephrons of a rat kidney. We simulated the inhibition of the Na(+)/H(+) exchanger (NHE3), the bumetanide-sensitive Na(+)-K(+)-2Cl(-) transporter (NKCC2), the Na(+)-Cl(-) cotransporter (NCC), and the amiloride-sensitive Na(+) channel (ENaC). Under baseline conditions, NHE3, NKCC2, NCC, and ENaC reabsorb 36, 22, 4, and 7%, respectively, of filtered Na(+) The model predicted that inhibition of NHE3 substantially reduced proximal tubule T(Na) and oxygen consumption (Q(O(2)) ). Whole-kidney T(Na) efficiency, as reflected by the number of moles of Na(+) reabsorbed per moles of O(2) consumed (denoted by the ratio T(Na)/Q(O(2)) ), decreased by approximately 20% with 80% inhibition of NHE3. NKCC2 inhibition simulations predicted a substantial reduction in thick ascending limb T(Na) and Q(O(2)) ; however, the effect on whole-kidney T(Na)/Q(O(2)) was minor. Tubular K(+) transport was also substantially impaired, resulting in elevated urinary K(+) excretion. The most notable effect of NCC inhibition was to increase the excretion of Na(+), K(+), and Cl(-); its impact on whole-kidney T(Na) and its efficiency was minor. Inhibition of ENaC was predicted to have opposite effects on the excretion of Na(+) (increased) and K(+) (decreased) and to have only a minor impact on whole-kidney T(Na) and T(Na)/Q(O(2)) Overall, model predictions agree well with measured changes in Na(+) and K(+) excretion in response to diuretics and Na(+) transporter mutations. Twit Text FOAVip Solute transport and oxygen consumption along the nephrons: effects of Na+ transport inhibitors ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27707706 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27707706 #FOAvip English Wikipedia <ref>{{Cite pmid|27707706}}</ref> Solute transport and oxygen consumption along the nephrons: effects of Na+ transport inhibitors #MMPMID27707706 Layton AT; Laghmani K; Vallon V; Edwards A Am J Physiol Renal Physiol 2016[Dec]; 311 (6): F1217-F1229 PMID27707706show ga Sodium and its associated anions are the major determinant of extracellular fluid volume, and the reabsorption of Na(+) by the kidney plays a crucial role in long-term blood pressure control. The goal of this study was to investigate the extent to which inhibitors of transepithelial Na(+) transport (T(Na)) along the nephron alter urinary solute excretion and T(Na) efficiency and how those effects may vary along different nephron segments. To accomplish that goal, we used the multinephron model developed in the companion study (28). That model represents detailed transcellular and paracellular transport processes along the nephrons of a rat kidney. We simulated the inhibition of the Na(+)/H(+) exchanger (NHE3), the bumetanide-sensitive Na(+)-K(+)-2Cl(-) transporter (NKCC2), the Na(+)-Cl(-) cotransporter (NCC), and the amiloride-sensitive Na(+) channel (ENaC). Under baseline conditions, NHE3, NKCC2, NCC, and ENaC reabsorb 36, 22, 4, and 7%, respectively, of filtered Na(+) The model predicted that inhibition of NHE3 substantially reduced proximal tubule T(Na) and oxygen consumption (Q(O(2)) ). Whole-kidney T(Na) efficiency, as reflected by the number of moles of Na(+) reabsorbed per moles of O(2) consumed (denoted by the ratio T(Na)/Q(O(2)) ), decreased by approximately 20% with 80% inhibition of NHE3. NKCC2 inhibition simulations predicted a substantial reduction in thick ascending limb T(Na) and Q(O(2)) ; however, the effect on whole-kidney T(Na)/Q(O(2)) was minor. Tubular K(+) transport was also substantially impaired, resulting in elevated urinary K(+) excretion. The most notable effect of NCC inhibition was to increase the excretion of Na(+), K(+), and Cl(-); its impact on whole-kidney T(Na) and its efficiency was minor. Inhibition of ENaC was predicted to have opposite effects on the excretion of Na(+) (increased) and K(+) (decreased) and to have only a minor impact on whole-kidney T(Na) and T(Na)/Q(O(2)) Overall, model predictions agree well with measured changes in Na(+) and K(+) excretion in response to diuretics and Na(+) transporter mutations. |*Models, Biological[MESH] |Animals[MESH] |Epithelial Sodium Channel Blockers/*pharmacology[MESH] |Ion Transport/drug effects[MESH] |Nephrons/*drug effects/metabolism[MESH] |Oxygen Consumption/*drug effects[MESH] |Rats[MESH] |Sodium-Hydrogen Exchanger 3[MESH] |Sodium-Hydrogen Exchangers/*antagonists & inhibitors[MESH]Solute transport and oxygen consumption along the nephrons: effects of(epmc).pdf DeepDyve Pubget Overpricing