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10.1681/ASN.2018080799 http://scihub22266oqcxt.onion/10.1681/ASN.2018080799 30559144!6362624!30559144     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2019 ; 30 (2): 216-227 Nephropedia Template TP {{tp|p=30559144|t=2019. Kir4 1/Kir5 1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter |pdf=|usr=}}{{30559144}} gab.com Text Kir4 1/Kir5 1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=30559144 #FOAvip BACKGROUND: Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Whether the basolateral, inwardly rectifying potassium channel Kir4.1/Kir5.1 (a heterotetramer of Kir4.1/Kir5.1) in the DCT is essential for mediating the effect of dietary sodium intake on NCC activity is unknown. METHODS: We used electrophysiology, renal clearance techniques, and immunoblotting to examine effects of Kir4.1/Kir5.1 in the DCT and NCC in wild-type and kidney-specific Kir4.1 knockout mice. RESULTS: Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K(+) conductance, and hyperpolarized the membrane. Conversely, high sodium intake inhibited the potassium channel, decreased basolateral K(+) currents, and depolarized the membrane. Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. In contrast, dietary sodium intake did not affect NCC activity in knockout mice. Further, Kir4.1 deletion not only abolished basolateral K(+) conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K(+) conductance and hyperpolarization. Finally, dietary sodium intake did not alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice. CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. Twit Text FOAVip Kir4 1/Kir5 1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=30559144 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30559144 #FOAvip English Wikipedia <ref>{{Cite pmid|30559144}}</ref> Kir4 1/Kir5 1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter #MMPMID30559144 Wu P; Gao ZX; Su XT; Wang MX; Wang WH; Lin DH J Am Soc Nephrol 2019[Feb]; 30 (2): 216-227 PMID30559144show ga BACKGROUND: Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Whether the basolateral, inwardly rectifying potassium channel Kir4.1/Kir5.1 (a heterotetramer of Kir4.1/Kir5.1) in the DCT is essential for mediating the effect of dietary sodium intake on NCC activity is unknown. METHODS: We used electrophysiology, renal clearance techniques, and immunoblotting to examine effects of Kir4.1/Kir5.1 in the DCT and NCC in wild-type and kidney-specific Kir4.1 knockout mice. RESULTS: Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K(+) conductance, and hyperpolarized the membrane. Conversely, high sodium intake inhibited the potassium channel, decreased basolateral K(+) currents, and depolarized the membrane. Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. In contrast, dietary sodium intake did not affect NCC activity in knockout mice. Further, Kir4.1 deletion not only abolished basolateral K(+) conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K(+) conductance and hyperpolarization. Finally, dietary sodium intake did not alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice. CONCLUSIONS: Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC. |Animals[MESH] |Disease Models, Animal[MESH] |Electrophysiology[MESH] |Hypokalemia/drug therapy/physiopathology[MESH] |Ion Transport[MESH] |Kidney Tubules, Distal/metabolism[MESH] |Membrane Potentials/*drug effects[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Natriuresis/drug effects[MESH] |Potassium Channels, Inwardly Rectifying/*genetics[MESH] |Random Allocation[MESH] |Receptors, Drug/drug effects[MESH] |Sensitivity and Specificity[MESH] |Sodium Chloride Symporters/drug effects[MESH] |Sodium, Dietary/*pharmacology[MESH] |Sodium-Potassium-Chloride Symporters/*drug effects/*metabolism[MESH]Kir4 1/Kir5 1 Activity Is Essential for Dietary Sodium Intake-Induced (epmc).pdf DeepDyve Pubget Overpricing