Background: Angiotensin-II (Ang-II) perfusion stimulates Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) and thiazide-sensitive Na-Cl-cotransporter (NCC).
View Article and Find Full Text PDFKey Points: Angiotensin II–type-1a-receptor in the distal convoluted tubule (DCT) plays a role in regulating sodium transport in the DCT. Angiotensin II–type-1a-receptor in the DCT plays a role in maintaining potassium homeostasis during sodium restriction.
Background: Chronic angiotensin II perfusion stimulates Kir4.
Calcineurin, protein phosphatase 2B (PP2B) or protein phosphatase 3 (PP3), is a calcium-dependent serine/threonine protein phosphatase. Calcineurin is widely expressed in the kidney and regulates renal Na and K transport. In the thick ascending limb, calcineurin plays a role in inhibiting NKCC2 function by promoting the dephosphorylation of the cotransporter and an intracellular sorting receptor, called sorting-related-receptor-with-A-type repeats (SORLA), is involved in modulating the effect of calcineurin on NKCC2.
View Article and Find Full Text PDFKey Points: High K stimulates mechanistic target of rapamycin complex 2 (mTORc2) in the distal convoluted tubule (DCT). Inhibition of mTORc2 decreased the basolateral Kir4.1/Kir5.
View Article and Find Full Text PDFHypertension
January 2024
Background: Kir4.2 and Kir4.1 play a role in regulating membrane transport in the proximal tubule (PT) and in the distal-convoluted-tubule (DCT), respectively.
View Article and Find Full Text PDFWe examine whether calcineurin or protein phosphatase 2B (PP2B) regulates the basolateral inwardly rectifying potassium channel Kir4.1/Kir5.1 in the distal convoluted tubule (DCT).
View Article and Find Full Text PDFCurr Opin Nephrol Hypertens
September 2022
Purpose Of Review: Kir5.1 interacts with Kir4.2 in proximal tubule and with Kir4.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
August 2022
The inwardly rectifying potassium channel (Kir) 4.1 (encoded by ) interacts with Kir5.1 (encoded by ) to form a major basolateral K channel in the renal distal convoluted tubule (DCT), connecting tubule (CNT), and the cortical collecting duct (CCD).
View Article and Find Full Text PDFAm J Physiol Renal Physiol
January 2022
We used whole cell recording to examine the renal outer medullary K channel (ROMK or Kir1.1) and epithelial Na channel (ENaC) in the late distal convoluted tubule (DCT2)/initial connecting tubule (CNT) and in the cortical collecting duct (CCD) of kidney tubule-specific neural precursor cell-expressed developmentally downregulated protein 4-2 (Nedd4-2) knockout mice (Ks-Nedd4-2 KO) and floxed neural precursor cell-expressed developmentally downregulated 4-like () mice (control). Tertiapin Q (TPNQ)-sensitive K currents (ROMK) were smaller in both the DCT2/CNT and CCD of Ks-Nedd4-2 KO mice on a normal diet than in control mice.
View Article and Find Full Text PDFHigh-dietary K (HK) intake inhibits basolateral Kir4.1/Kir5.1 activity in the distal convoluted tubule (DCT), and HK-induced inhibition of Kir4.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
June 2021
High sodium (HS) intake inhibited epithelial Na channel (ENaC) in the aldosterone-sensitive distal nephron and Na-Cl cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT), thereby increasing renal Na excretion but not affecting K excretion.
View Article and Find Full Text PDFNeural precursor cell expressed developmentally downregulated protein 4-2 (Nedd4-2) regulates the expression of Kir4.1, thiazide-sensitive NaCl cotransporter (NCC), and epithelial Na channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN), and Nedd4-2 deletion causes salt-sensitive hypertension. We now examined whether Nedd4-2 deletion compromises the effect of high-salt (HS) diet on Kir4.
View Article and Find Full Text PDFBackground Angiotensin II stimulates epithelial Na channel (ENaC) by aldosterone-independent mechanism. We now test the effect of angiotensin II on ENaC in the distal convoluted tubule (DCT) and cortical collecting duct (CCD) of wild-type (WT) and kidney-specific mineralocorticoid receptor knockout mice (KS-MR-KO). Methods and Results We used electrophysiological, immunoblotting and renal-clearance methods to examine the effect of angiotensin II on ENaC in KS-MR-KO and wild-type mice.
View Article and Find Full Text PDFThe 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).
View Article and Find Full Text PDFHypomagnesemia is associated with reduced kidney function and life-threatening complications and sustains hypokalemia. The distal convoluted tubule (DCT) determines final urinary Mg excretion and, via activity of the Na-Cl cotransporter (NCC), also plays a key role in K homeostasis by metering Na delivery to distal segments. Little is known about the mechanisms by which plasma Mg concentration regulates NCC activity and how low-plasma Mg concentration and K concentration interact to modulate NCC activity.
View Article and Find Full Text PDFBackground: The basolateral potassium channel in the distal convoluted tubule (DCT), comprising the inwardly rectifying potassium channel Kir4.1/Kir5.1 heterotetramer, plays a key role in mediating the effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC).
View Article and Find Full Text PDFThe stimulation of β-adrenergic receptor increases thiazide-sensitive NaCl cotransporter (NCC), an effect contributing to salt-sensitive hypertension by sympathetic stimulation. We now test whether the stimulation of β-adrenergic receptor-induced activation of NCC is achieved through activating basolateral Kir4.1 in the distal convoluted tubule (DCT).
View Article and Find Full Text PDFBackground: 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.
View Article and Find Full Text PDFStimulation of BK2R (bradykinin [BK] B2 receptor) has been shown to increase renal Na excretion. The aim of the present study is to explore the role of BK2R in regulating Kir4.1 and NCC (NaCl cotransporter) in the distal convoluted tubule (DCT).
View Article and Find Full Text PDFAm J Physiol Renal Physiol
October 2018
Kir4.1/5.1 heterotetramer participates in generating the negative cell membrane potential in distal convoluted tubule (DCT) and plays a critical role in determining the activity of Na-Cl cotransporter (NCC).
View Article and Find Full Text PDFAT2R (AngII [angiotensin II] type 2 receptor) is expressed in the distal nephrons. The aim of the present study is to examine whether AT2R regulates NCC (Na-Cl cotransporter) and Kir4.1 of the distal convoluted tubule.
View Article and Find Full Text PDFKir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we tested whether dietary potassium intake modulates Kir4.
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