50 results on '"Duan, Xin‐Peng"'
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2. mTORc2 in Distal-Convoluted-Tubule and Renal K+-Excretion during High Dietary K+ Intake
3. Hypomagnesemia-induced Hypokalemia Is Associated with Higher Activities of ENaC and ROMK
4. Potassium Activates mTORC2-dependent SGK1 Phosphorylation to Stimulate Epithelial Sodium Channel: Role in Rapid Renal Responses to Dietary Potassium
5. Role of calcineurin in regulating renal potassium (K+) excretion: Mechanisms of calcineurin inhibitor‐induced hyperkalemia.
6. Role of Angiotensin II Type 1a Receptor (AT1aR) of Renal Tubules in Regulating Inwardly Rectifying Potassium Channels 4.2 (Kir4.2), Kir4.1, and Epithelial Na + Channel (ENaC)
7. Role of inwardly rectifying K+ channel 5.1 (Kir5.1) in the regulation of renal membrane transport
8. Dietary potassium restriction reprograms the distal tubule causing adverse metabolic consequences
9. Potassium Activates mTORC2-dependent SGK1 Phosphorylation to Stimulate ENaC: Role in Rapid Renal Responses to Dietary Potassium
10. Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule
11. Calcineurin-inhibitors stimulate Kir4.1/Kir5.1 of distal-convoluted-tubule to increase Na-Cl cotransporter (NCC)
12. Bradykinin Stimulates Renal Na+ and K+ Excretion by Inhibiting the K+ Channel (Kir4.1) in the Distal Convoluted Tubule
13. The effect of high-dietary K+ (HK) on Kir4.1/Kir5.1 and ROMK in the distal convoluted tubule (DCT) is not affected by gender and Cl− content of the diet
14. Mineralocorticoid Receptor Antagonists Cause Natriuresis in the Absence of Aldosterone
15. Activation of Kir4.1/Kir5.1 of DCT is essential for acute calcineurin‐inhibition‐induced stimulation of NCC
16. ROMK channels are inhibited in the aldosterone-sensitive distal nephron of renal tubule Nedd4-2-deficient mice
17. Deletion of renal Nedd4-2 abolishes the effect of high K+ intake on Kir4.1/Kir5.1 and NCC activity in the distal convoluted tubule
18. Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl− cotransporter
19. Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS
20. Role of inwardly rectifying K+channel 5.1 (Kir5.1) in the regulation of renal membrane transport
21. Epoxyeicosatrienoic acid metabolites inhibit Kir4.1/Kir5.1 in the distal convoluted tubule
22. Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule
23. Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice
24. Kir4.1/Kir5.1 Activity in the DCT is Essential for Angiotensin II Induced Stimulation of Thiazide‐Sensitive NCC Expression/Activity.
25. Role of Mineralocorticoid receptor (MR) and NEDD4‐2 in the regulation of ENaC and ROMK in the Distal Convoluted Tubule (DCT) and Cortical Collecting Duct (CCD)
26. Deletion of NEDD4‐2 Abolishes the Inhibitory Effect of High Sodium (HS) Intake on the Basolateral Kir4.1/Kir5.1 of the DCT and Thiazide‐Sensitive Na‐Cl Cotransport (NCC)
27. AT2R-mediated regulation of Na-Cl cotransporter (NCC) and renal K excretion depends on the K channel, Kir4.1
28. Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule
29. Deletion of renal Nedd4-2 abolishes the effect of high K+intake on Kir4.1/Kir5.1 and NCC activity in the distal convoluted tubule
30. Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice.
31. Bradykinin Stimulates Renal Na + and K + Excretion by Inhibiting the K + Channel (Kir4.1) in the Distal Convoluted Tubule
32. AT2R (Angiotensin II Type 2 Receptor)-Mediated Regulation of NCC (Na-Cl Cotransporter) and Renal K Excretion Depends on the K Channel, Kir4.1
33. Bradykinin Stimulates Renal Na+ and K+ Excretion by Inhibiting the K+ Channel (Kir4.1) in the Distal Convoluted Tubule.
34. AT2R (Angiotensin II Type 2 Receptor)-Mediated Regulation of NCC (Na-Cl Cotransporter) and Renal K Excretion Depends on the K Channel, Kir4.1.
35. ROMK channels are inhibited in the aldosterone-sensitive distal nephron (ASDN) of renal-tubule Nedd4-2 deficient mice.
36. Role of calcineurin in regulating renal potassium (K + ) excretion: Mechanisms of calcineurin inhibitor-induced hyperkalemia.
37. Role of Kir4.1/Kir5.1 in mediating Angiotensin-II (Ang-II)-induced stimulation of thiazide-sensitive Na-Cl cotransporter.
38. Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.
39. mTORc2 in Distal Convoluted Tubule and Renal K + Excretion during High Dietary K + Intake.
40. [Recording and identification of depolarization-activated current in intercalated cells].
41. Calcineurin inhibitors stimulate Kir4.1/Kir5.1 of the distal convoluted tubule to increase NaCl cotransporter.
42. The effect of high-dietary K + (HK) on Kir4.1/Kir5.1 and ROMK in the distal convoluted tubule (DCT) is not affected by gender and Cl - content of the diet.
43. ROMK channels are inhibited in the aldosterone-sensitive distal nephron of renal tubule Nedd4-2-deficient mice.
44. Deletion of renal Nedd4-2 abolishes the effect of high K + intake on Kir4.1/Kir5.1 and NCC activity in the distal convoluted tubule.
45. Deletion of Kir5.1 abolishes the effect of high Na + intake on Kir4.1 and Na + -Cl - cotransporter.
46. Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS.
47. Epoxyeicosatrienoic acid metabolites inhibit Kir4.1/Kir5.1 in the distal convoluted tubule.
48. [Progress of renal distal convoluted tubule Na-Cl cotransporter].
49. [Posttranslational modification and expression regulation of aquporin AQP2].
50. [The role of Epac in kidney tuble physiology].
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