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10.1152/ajprenal.00436.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00436.2015 26632606!4839479!26632606     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 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 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 310 (4): F311-21 Nephropedia Template TP {{tp|p=26632606|t=2016. Insulin and IGF-1 activate Kir4 1/5 1 channels in cortical collecting duct principal cells to control basolateral membrane voltage |pdf=|usr=}}{{26632606}} gab.com Text Insulin and IGF-1 activate Kir4 1/5 1 channels in cortical collecting duct principal cells to control basolateral membrane voltage JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26632606 #FOAvip Potassium Kir4.1/5.1 channels are abundantly expressed at the basolateral membrane of principal cells in the cortical collecting duct (CCD), where they are thought to modulate transport rates by controlling transepithelial voltage. Insulin and insulin-like growth factor-1 (IGF-1) stimulate apically localized epithelial sodium channels (ENaC) to augment sodium reabsorption in the CCD. However, little is known about their actions on potassium channels localized at the basolateral membrane. In this study, we implemented patch-clamp analysis in freshly isolated murine CCD to assess the effect of these hormones on Kir4.1/5.1 at both single channel and cellular levels. We demonstrated that K(+)-selective conductance via Kir4.1/5.1 is the major contributor to the macroscopic current recorded from the basolateral side in principal cells. Acute treatment with 10 muM amiloride (ENaC blocker), 100 nM tertiapin-Q (TPNQ; ROMK inhibitor), and 100 muM ouabain (Na(+)-K(+)-ATPase blocker) failed to produce a measurable effect on the macroscopic current. In contrast, Kir4.1 inhibitor nortriptyline (100 muM), but not fluoxetine (100 muM), virtually abolished whole cell K(+)-selective conductance. Insulin (100 nM) markedly increased the open probability of Kir4.1/5.1 and nortriptyline-sensitive whole cell current, leading to significant hyperpolarization of the basolateral membrane. Inhibition of the phosphatidylinositol 3-kinase cascade with LY294002 (20 muM) abolished action of insulin on Kir4.1/5.1. IGF-1 had similar stimulatory actions on Kir4.1/5.1-mediated conductance only when applied at a higher (500 nM) concentration and was ineffective at 100 nM. We concluded that both insulin and, to a lesser extent, IGF-1 activate Kir4.1/5.1 channel activity and open probability to hyperpolarize the basolateral membrane, thereby facilitating Na(+) reabsorption in the CCD. Twit Text FOAVip Insulin and IGF-1 activate Kir4 1/5 1 channels in cortical collecting duct principal cells to control basolateral membrane voltage ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26632606 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26632606 #FOAvip English Wikipedia <ref>{{Cite pmid|26632606}}</ref> Insulin and IGF-1 activate Kir4 1/5 1 channels in cortical collecting duct principal cells to control basolateral membrane voltage #MMPMID26632606 Zaika O; Palygin O; Tomilin V; Mamenko M; Staruschenko A; Pochynyuk O Am J Physiol Renal Physiol 2016[Feb]; 310 (4): F311-21 PMID26632606show ga Potassium Kir4.1/5.1 channels are abundantly expressed at the basolateral membrane of principal cells in the cortical collecting duct (CCD), where they are thought to modulate transport rates by controlling transepithelial voltage. Insulin and insulin-like growth factor-1 (IGF-1) stimulate apically localized epithelial sodium channels (ENaC) to augment sodium reabsorption in the CCD. However, little is known about their actions on potassium channels localized at the basolateral membrane. In this study, we implemented patch-clamp analysis in freshly isolated murine CCD to assess the effect of these hormones on Kir4.1/5.1 at both single channel and cellular levels. We demonstrated that K(+)-selective conductance via Kir4.1/5.1 is the major contributor to the macroscopic current recorded from the basolateral side in principal cells. Acute treatment with 10 muM amiloride (ENaC blocker), 100 nM tertiapin-Q (TPNQ; ROMK inhibitor), and 100 muM ouabain (Na(+)-K(+)-ATPase blocker) failed to produce a measurable effect on the macroscopic current. In contrast, Kir4.1 inhibitor nortriptyline (100 muM), but not fluoxetine (100 muM), virtually abolished whole cell K(+)-selective conductance. Insulin (100 nM) markedly increased the open probability of Kir4.1/5.1 and nortriptyline-sensitive whole cell current, leading to significant hyperpolarization of the basolateral membrane. Inhibition of the phosphatidylinositol 3-kinase cascade with LY294002 (20 muM) abolished action of insulin on Kir4.1/5.1. IGF-1 had similar stimulatory actions on Kir4.1/5.1-mediated conductance only when applied at a higher (500 nM) concentration and was ineffective at 100 nM. We concluded that both insulin and, to a lesser extent, IGF-1 activate Kir4.1/5.1 channel activity and open probability to hyperpolarize the basolateral membrane, thereby facilitating Na(+) reabsorption in the CCD. |Animals[MESH] |Cell Membrane/*drug effects[MESH] |Dose-Response Relationship, Drug[MESH] |Electrophysiological Phenomena/drug effects[MESH] |Hypoglycemic Agents/*pharmacology[MESH] |Insulin-Like Growth Factor I/antagonists & inhibitors/*pharmacology[MESH] |Insulin/*pharmacology[MESH] |Kidney Tubules, Collecting/chemistry/drug effects/*metabolism[MESH] |Kir5.1 Channel[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Patch-Clamp Techniques[MESH] |Phosphoinositide-3 Kinase Inhibitors[MESH] |Potassium Channel Blockers/pharmacology[MESH] |Potassium Channels, Inwardly Rectifying/agonists/*metabolism[MESH]Insulin and IGF-1 activate Kir4 1/5 1 channels in cortical collecting (epmc).pdf DeepDyve Pubget Overpricing