Effects of Glyburide on Renal Tubule Transport and Potassium-Channel Activity

Wang, Tong; Wang, Wenhui; Klein-Robbenhaar, Geertruida; Giebisch, Gerhard

doi:10.1159/000173914

Cited by 33 publications

(57 citation statements)

References 18 publications

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“…Mg-ATP concentrations of ≥1 mM and micromolar concentrations of the sulfonylurea glibenclamide inhibit the 30 pS K channels in the TAL and CCD (19). In vitro studies have suggested that CFTR may be required for inhibition of ROMK by cytosolic ATP (20) and glibenclamide (20,21).…”

Section: Introductionmentioning

confidence: 99%

CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney

Li²,

Egan³

et al. 2006

Journal of Clinical Investigation

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The cystic fibrosis transmembrane conductance regulator (CFTR) Cl -channel plays vital roles in fluid transport in many epithelia. While CFTR is expressed along the entire nephron, its function in renal tubule epithelial cells remains unclear, as no specific renal phenotype has been identified in cystic fibrosis. CFTR has been proposed as a regulator of the 30 pS, ATP-sensitive renal K channel (Kir1.1, also known as renal outer medullar K [ROMK]) that is critical for K secretion by cells of the thick ascending limb (TAL) and distal nephron segments responsive to aldosterone. We report here that both ATP and glibenclamide sensitivities of the 30 pS K channel in TAL cells were absent in mice lacking CFTR and in mice homozygous for the ΔF508 mutation. Curcumin treatment in ΔF508-CFTR mice partially reversed the defect in ATP sensitivity. We demonstrate that the effect of CFTR on ATP sensitivity was abrogated by increasing PKA activity. We propose that CFTR regulates the renal K secretory channel by providing a PKA-regulated functional switch that determines the distribution of open and ATP-inhibited K channels in apical membranes. We discuss the potential physiological role of this functional switch in renal K handling during water diuresis and the relevance to renal K homeostasis in cystic fibrosis.

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Section: Introductionmentioning

confidence: 99%

CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney

Li²,

Egan³

et al. 2006

Journal of Clinical Investigation

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“…Glibenclamide inhibited the transport of Na + and K + in the ascending thick limb of Henle's loop by blocking K + recycling across the apical membrane. 21 This inhibition led to the delivery of the large amounts of fluid and Na + at the initial and cortical collecting tubule. 31 This action was similar to a loop diuretic such as furosemide.…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that glibenclamide inhibited the transporter of Na + and K + in the ascending thick limb of Henle's loop by blocking K + recycling across the apical membrane. 21 In addition, inhibition of K + secretion in the collecting tubules occurred by decreasing the activity of apical K + channels preventing kaliuresis. 21 A kidneyselective ATP-sensitive potassium channel blocker, U18177 and its 1-adamantyl analog (U37883A) were developed as diuretics and as more selective blockers of the kidney ATP-sensitive channel.…”

Section: Introductionmentioning

confidence: 99%

“…21 In addition, inhibition of K + secretion in the collecting tubules occurred by decreasing the activity of apical K + channels preventing kaliuresis. 21 A kidneyselective ATP-sensitive potassium channel blocker, U18177 and its 1-adamantyl analog (U37883A) were developed as diuretics and as more selective blockers of the kidney ATP-sensitive channel. 22,23 Glibenclamide and U37883A also dose-dependently accelerated the secretion of kallikrein from the kidney.…”

Section: Introductionmentioning

confidence: 99%

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An ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein

et al. 2009

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It is suggested that an ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein. We reported that glibenclamide, an ATP-sensitive potassium channel blocker, accelerated dose-dependent secretion of renal kallikrein in sliced kidney cortex and in vivo in rats. In vehicle-treated normal BrownNorway-Kitasato (nBN-Ki) rats, the administration of glibenclamide increased urinary kallikrein secretion, but changed neither the systolic blood pressure nor the urinary sodium on low (0.3%) NaCl diets. Although on high (8%) NaCl diets, the systolic blood pressure of the nBN-Ki rats administrated glibenclamide was significantly lower (Po0.05). The urinary levels of kallikrein and sodium of the nBN-Ki rats administrated glibenclamide were significantly increased (Po0.05, glibenclamide vs. vehicle). A similar result was obtained with a kidney-selective ATP-sensitive potassium blocker, N,N¢-dicyclohexyl-4-morpholinecarboxamidine (U18177), in SD rats. Mutant kininogen-deficient Brown-Norway Katholiek (muBN-Ka) rats fed high (8%) NaCl diets showed an increase in urinary kallikrein levels, but showed neither hypotensive nor natriuretic actions by glibenclamide. A bradykinin B 2 receptor antagonist,-dichlorobenzyloxy]-2-methylquinoline (FR173657), which was administrated to SD rats, together with glibenclamide, abolished the hypotensive and natriuretic effects of glibenclamide in high-sodium (8%NaCl) hypertension, despite an accelerated secretion of urinary kallikrein. Therefore, these results indicate that glibenclamide, an ATP-sensitive potassium channel blocker suppressed sodium-induced hypertension through sodium excretion from the kidney resulting from accelerated secretion of urinary kallikrein.

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“…Reminiscent of K ATP channels in excitable tissues, which are heteromultimeric proteins complexes comprised regulatory sulfonylurea receptor (SUR) 1 ATP-binding cassette gene products and pore-forming inward rectifier, Kir 6 subunits (12,13), present evidence from molecular reconstitution studies indicates that ROMK channels also require a ATP-binding cassette protein cofactor to manifest native channel properties. We and others found that coexpression of CFTR with ROMK in Xenopus oocytes leads to the formation of weakly inward rectifying channels that have acquired sensitivity to sulfonylurea agents (14) and ATP-dependent gating properties (15) like the native channel (16,17). With observations that the expression patterns of ROMK (2)(3)(4) and CFTR (18) overlap along the thick ascending limb and collecting duct apical membrane, it seems plausible that the native ROMK secretory channel may be regulated by CFTR in the kidney.…”

mentioning

confidence: 99%

Assembly and Trafficking of a Multiprotein ROMK (Kir 1.1) Channel Complex by PDZ Interactions

Yoo

Flagg

Olsen

et al. 2004

Journal of Biological Chemistry

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The ROMK subtypes of inward rectifier K ؉ channels (Kir 1.1, KCNJ1) mediate potassium secretion and regulate NaCl reabsorption in the kidney. In the present study, the role of the PDZ binding motif in ROMK function is explored. Here we identify the Na/H exchange regulatory factors, NHERF-1 and NHERF-2, as PDZ domain interaction partners of the ROMK channel. Characterization of the basis and consequences of NHERF association with ROMK reveals a PDZ interaction-dependent trafficking process and a coupling mechanism for linking ROMK to a channel modifier protein, the cystic fibrosis transmembrane regulator (CFTR). As

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Effects of Glyburide on Renal Tubule Transport and Potassium-Channel Activity

Cited by 33 publications

References 18 publications

CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney

CFTR is required for PKA-regulated ATP sensitivity of Kir1.1 potassium channels in mouse kidney

An ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein

Assembly and Trafficking of a Multiprotein ROMK (Kir 1.1) Channel Complex by PDZ Interactions

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