A5054866260- Ion Transport and Channel Regulation
- Ion channel regulation and function
- Electrolyte and hormonal disorders
- Hormonal Regulation and Hypertension
- Magnesium in Health and Disease
- Potassium and Related Disorders
- Sodium Intake and Health
- Neuroendocrine regulation and behavior
- Barrier Structure and Function Studies
- Signaling Pathways in Disease
- Chemical Synthesis and Reactions
- Planarian Biology and Electrostimulation
- Phytochemical Studies and Bioactivities
- Glutathione Transferases and Polymorphisms
- Apelin-related biomedical research
- Dietary Effects on Health
- Analytical Chemistry and Sensors
- Ion Channels and Receptors
- Biomedical Research and Pathophysiology
- Cardiac electrophysiology and arrhythmias
- Acupuncture Treatment Research Studies
- Healthcare and Venom Research
- Eicosanoids and Hypertension Pharmacology
- Electromagnetic Fields and Biological Effects
- Synthesis and Characterization of Pyrroles
Xuzhou Medical College
2021-2025
New York Medical College
2018-2025
Zero to Three
2024
Harbin Medical University
2013-2018
Significance Statement Rapid renal responses to ingested potassium are essential prevent hyperkalemia and also play a central role in blood pressure regulation. Although local extracellular K + concentration kidney tissue is increasingly recognized as an important regulator of secretion, the underlying mechanisms that relevant vivo remain controversial. To assess signaling kinase mTOR complex-2 (mTORC2), authors compared effects administered by gavage wild-type mice knockout with...
Background Angiotensin II stimulates epithelial Na + channel (ENaC) by aldosterone‐independent mechanism. We now test the effect of angiotensin on ENaC in distal convoluted tubule (DCT) and cortical collecting duct (CCD) wild‐type (WT) kidney‐specific mineralocorticoid receptor knockout mice (KS‐MR‐KO). Methods Results used electrophysiological, immunoblotting renal‐clearance methods to examine KS‐MR‐KO mice. High K intake stimulated late DCT/early connecting (DCT2/CNT) CCD whereas low...
Background: MR (mineralocorticoid receptor) antagonists are recommended for patients with resistant hypertension even when circulating aldosterone levels not high. Although activates to increase epithelial sodium channel (ENaC) activity, glucocorticoids also activate but metabolized by 11βHSD2 (11β-hydroxysteroid dehydrogenase type 2). is expressed at increasing from distal convoluted tubule (DCT) through collecting duct. Here, we hypothesized that maintains ENaC activity in the DCT2 and...
Kir5.1 encoded by
Kidney thick ascending limb cells reabsorb sodium, potassium, calcium, and magnesium contribute to urinary concentration. These are typically viewed as of a single type that recycles potassium across the apical membrane generates lumen-positive transepithelial voltage driving calcium reabsorption, although variability in channel expression has been reported. Additionally, recent transcriptomic analyses suggest different cell types exist along this segment, but classifications have varied not...
Stimulation of BK2R (bradykinin [BK] B2 receptor) has been shown to increase renal Na + excretion. The aim the present study is explore role in regulating Kir4.1 and NCC (NaCl cotransporter) distal convoluted tubule (DCT). Immunohistochemical studies demonstrated that was highly expressed both apical lateral membrane Kir4.1-positive tubules, such as DCT. Patch-clamp experiments BK inhibited basolateral 40-pS K channel (a Kir4.1/5.1 heterotetramer) DCT, this effect blocked by antagonist but...
Significance Statement The potassium channel Kir4.1 forms the Kir4.1/Kir5.1 heterotetramer in basolateral membrane of distal convoluted tubule (DCT) and plays an important role regulating thiazide-sensitive NaCl cotransporter (NCC). Deletion ubiquitin ligase Nedd4-2 has been shown to increase expression NCC cause salt-sensitive hypertension. authors demonstrated that kidney-specific deletion mice also stimulates activity DCT hyperpolarizes membrane. They found activity/expression is largely...
Neural 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 aldosterone-sensitive distal nephron (ASDN), Nedd4-2 deletion causes salt-sensitive hypertension. We now examined whether compromises effect high-salt (HS) diet on NCC, ENaC, renal K+ excretion. Immunoblot analysis showed that HS decreased Ca2+-activated large-conductance subunit-α (BKα),...
The 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 receptor-induced activation NCC is achieved through activating basolateral Kir4.1 in distal convoluted tubule (DCT). Application norepinephrine increased 40 pS K
We examine whether calcineurin or protein phosphatase 2B (PP2B) regulates the basolateral inwardly rectifying potassium channel Kir4.1/Kir5.1 in distal convoluted tubule (DCT). Application of tacrolimus (FK506) cyclosporine A (CsA) increased whole-cell Kir4.1/Kir5.1-mediated K+ currents and hyperpolarized DCT membrane. Moreover, FK506-induced stimulation was absent kidney tubule-specific 12 kDa FK506-binding protein-knockout mice (Ks-FKBP-12-KO). In contrast, CsA stimulated Ks-FKBP-12-KO...
AT2R (AngII [angiotensin II] type 2 receptor) is expressed in the distal nephrons. The aim of present study to examine whether regulates NCC (Na-Cl cotransporter) and Kir4.1 convoluted tubule. AngII inhibited basolateral 40 pS K channel (a Kir4.1/5.1 heterotetramer) tubule treated with losartan but not PD123319. agonist also inhibits channel, indicating that was involved tonic regulation Kir4.1. infusion PD123319 stimulated expression tNCC (total NCC) pNCC (phosphorylated NCC; Thr
Kir5.1 plays an important role in mediating the effect of high sodium intake on basolateral K + channels distal convoluted tubule and Na -Cl − cotransporter activity/expression.
Key Points High K stimulates mechanistic target of rapamycin complex 2 (mTORc2) in the distal convoluted tubule (DCT). Inhibition mTORc2 decreased basolateral Kir4.1/Kir5.1 and Na-Cl cotransporter DCT. DCT compromised kidneys' ability to excrete potassium during high intake. Background Renal plays a role regulating renal + excretion (renal-E ) homeostasis. causes hyperkalemia due suppressing epithelial Na channel outer medullary K+ (Kir1.1) collecting duct. We now explore whether tubules...
High-dietary K+ (HK) intake inhibits basolateral Kir4.1/Kir5.1 activity in the distal convoluted tubule (DCT), and HK-induced inhibition of is essential for NaCl cotransporter (NCC). Here, we examined whether neural precursor cell expressed developmentally downregulated 4-2 (Nedd4-2) deletion compromises effect HK on NCC DCT. Single-channel recording whole showed that neither decreased nor low-dietary (LK) increased DCT kidney tubule-specific Nedd4-2 knockout (Ks-Nedd4-2 KO) mice. In...
BACKGROUND: Kir4.2 and Kir4.1 play a role in regulating membrane transport the proximal tubule (PT) distal-convoluted-tubule (DCT), respectively. METHODS: We generated kidney-tubule-specific-AT1aR-knockout (Ks-AT1aR-KO) mice to examine whether renal AT1aR regulates Kir4.1. RESULTS: Ks-AT1aR-KO had lower systolic blood pressure than Agtr1a flox/flox (control) mice. expression of NHE 3 (Na + /H -exchanger 3) Kir4.2, major Kir-channel PT, Whole-cell recording also demonstrated that potential PT...
We used whole cell recording to examine the renal outer medullary K
We used the patch-clamp technique to examine effect of angiotensin II (ANG II) on basolateral K channels in thick ascending limb (TAL) rat kidney. Application ANG increased channel activity and current amplitude 50-pS channel. The stimulatory was completely abolished by losartan, an inhibitor type 1 receptor (AT R), but not PD123319, AT 2 R antagonist. Moreover, inhibition phospholipase C (PLC) protein kinase (PKC) also abrogated TAL. This suggests that induced activating PLC PKC pathways....
Background: Hypokalemia occurs in 40 to 60% of patients with hypomagnesemia, and can result cardiac arrhythmia sudden death. Along the distal nephron, a decrease intracellular Mg 2+ has been proposed release -mediated inhibition renal outer medullary K + (ROMK) channels, increasing urinary excretion. However, hypomagnesemia alone is not suffcient cause hypokalemia. Higher activity epithelial Na channel (ENaC), which provides driving force for secretion via ROMK, be an additional requirement....
Background: The mTORc2 is a multiprotein complex and the core components of contain mTOR (a serine/threonine protein kinase) RICTOR (rapamycin insensitive companion mTOR). Previous studies have strongly suggested role in regulation renal K + excretion by stimulating epithelial Na channels (ENaC) ROMK (Kir1.1) aldosterone-sensitive distal nephron (ASDN). mice with deletion or tubules are hyperkalemic during increasing dietary intake. A large body evidence has demonstrated that HK-induced...
Key Points Angiotensin II–type-1a-receptor in the distal convoluted tubule (DCT) plays a role regulating sodium transport DCT. DCT maintaining potassium homeostasis during restriction. Background Chronic angiotensin II perfusion stimulates Kir4.1/Kir5.1 of via (AT1aR), and low‐sodium intake also Kir4.1/Kir5.1. However, AT1aR mediating effect low salt on is not explored. Methods We used patch-clamp technique to examine activity DCT, employed immunoblotting Na-Cl cotransporter (NCC)...