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10.1161/HYPERTENSIONAHA.119.13852 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.119.13852 31865783!7561014!31865783     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2020 ; 75 (2): 439-448 Nephropedia Template TP {{tp|p=31865783|t=2020. Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High K(+) Intake-Induced Renal K(+) Excretion |pdf=|usr=}}{{31865783}} gab.com Text Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High K(+) Intake-Induced Renal K(+) Excretion JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=31865783 #FOAvip The inhibition of Type II angiotensin II receptor (AT2R) or BK2R (bradykinin type II receptor) stimulates basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT) and activates thiazide-sensitive NCC (Na-Cl cotransporter). The aim of the present study is to examine the role of AT2R and BK2R in mediating the effect of HK (high dietary K(+)) intake on the basolateral K(+) channels, NCC, and renal K(+) excretion. Feeding mice (male and female) with HK diet for overnight significantly decreased the basolateral K(+) conductance, depolarized the DCT membrane, diminished the expression of pNCC (phosphorylated NCC) and tNCC (total NCC), and decreased thiazide-sensitive natriuresis. Overnight HK intake also increased the expression of cleaved ENaC-alpha and -gamma subunits but had no effect on NKCC2 expression. Pretreatment of the mice (male and female) with PD123319 and HOE140 stimulated the expression of tNCC and pNCC, augmented hydrochlorothiazide-induced natriuresis, and increased the negativity of the DCT membrane. The deletion of Kir4.1 not only decreased the NCC activity but also abolished the stimulatory effect of PD123319 and HOE140 perfusion on NCC activity. Moreover, the effect of overnight HK loading on Kir4.1/Kir5.1 in the DCT and NCC expression/activity was compromised in the mice treated with AT2R/BK2R antagonists. Renal clearance study showed that inhibition of AT2R and BK2R impairs renal K(+) excretion in response to overnight HK loading, and the mice pretreated with PD123319 and HOE140 were hyperkalemic during HK intake. We conclude that synergistic activation of AT2R and BK2R is required for the effect of overnight HK diet on Kir4.1/Kir5.1 in the DCT and NCC activity. Twit Text FOAVip Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High K(+) Intake-Induced Renal K(+) Excretion ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=31865783 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31865783 #FOAvip English Wikipedia <ref>{{Cite pmid|31865783}}</ref> Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises High K(+) Intake-Induced Renal K(+) Excretion #MMPMID31865783 Gu L; Wang J; Zhang DD; Meng X; Zhang Y; Zhang J; Zhang H; Guo X; Lin DH; Wang WH; Gu RM Hypertension 2020[Feb]; 75 (2): 439-448 PMID31865783show ga The inhibition of Type II angiotensin II receptor (AT2R) or BK2R (bradykinin type II receptor) stimulates basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT) and activates thiazide-sensitive NCC (Na-Cl cotransporter). The aim of the present study is to examine the role of AT2R and BK2R in mediating the effect of HK (high dietary K(+)) intake on the basolateral K(+) channels, NCC, and renal K(+) excretion. Feeding mice (male and female) with HK diet for overnight significantly decreased the basolateral K(+) conductance, depolarized the DCT membrane, diminished the expression of pNCC (phosphorylated NCC) and tNCC (total NCC), and decreased thiazide-sensitive natriuresis. Overnight HK intake also increased the expression of cleaved ENaC-alpha and -gamma subunits but had no effect on NKCC2 expression. Pretreatment of the mice (male and female) with PD123319 and HOE140 stimulated the expression of tNCC and pNCC, augmented hydrochlorothiazide-induced natriuresis, and increased the negativity of the DCT membrane. The deletion of Kir4.1 not only decreased the NCC activity but also abolished the stimulatory effect of PD123319 and HOE140 perfusion on NCC activity. Moreover, the effect of overnight HK loading on Kir4.1/Kir5.1 in the DCT and NCC expression/activity was compromised in the mice treated with AT2R/BK2R antagonists. Renal clearance study showed that inhibition of AT2R and BK2R impairs renal K(+) excretion in response to overnight HK loading, and the mice pretreated with PD123319 and HOE140 were hyperkalemic during HK intake. We conclude that synergistic activation of AT2R and BK2R is required for the effect of overnight HK diet on Kir4.1/Kir5.1 in the DCT and NCC activity. |Animals[MESH] |Biological Transport[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Hyperkalemia/*metabolism/pathology[MESH] |Immunoblotting[MESH] |Kidney Tubules, Distal/*metabolism/pathology[MESH] |Male[MESH] |Membrane Potentials[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Potassium/*metabolism[MESH] |Receptor, Bradykinin B2/drug effects/*metabolism[MESH]Inhibition of AT2R and Bradykinin Type II Receptor (BK2R) Compromises (epmc).pdf DeepDyve Pubget Overpricing