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  • 1
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    Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of the American Heart Association Vol. 9, No. 7 ( 2020-04-09)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 9, No. 7 ( 2020-04-09)
    Abstract: 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. High K + intake stimulated ENaC in the late DCT/early connecting tubule (DCT2/CNT) and in the CCD whereas low sodium intake stimulated ENaC in the CCD but not in the DCT2/CNT. The deletion of MR abolished the stimulatory effect of high K + and low sodium intake on ENaC, partially inhibited ENaC in DCT2/CNT but almost abolished ENaC activity in the CCD. Application of losartan inhibited ENaC only in DCT2/CNT of both wild‐type and KS‐MR‐KO mice but not in the CCD. Angiotensin II infusion for 3 days has a larger stimulatory effect on ENaC in the DCT2/CNT than in the CCD. Three lines of evidence indicate that angiotensin II can stimulate ENaC by MR‐independent mechanism: (1) angiotensin II perfusion augmented ENaC expression in KS‐MR‐KO mice; (2) angiotensin II stimulated ENaC in the DCT2/CNT but to a lesser degree in the CCD in KS‐MR‐KO mice; (3) angiotensin II infusion augmented benzamil‐induced natriuresis, increased the renal K + excretion and corrected hyperkalemia of KS‐MR‐KO mice. Conclusions Angiotensin II‐induced stimulation of ENaC occurs mainly in the DCT2/CNT and to a lesser degree in the CCD and MR plays a dominant role in determining ENaC activity in the CCD but to a lesser degree in the DCT2/CNT.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.119.014996
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 2
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    Bradykinin Stimulates Renal Na + and K + Excretion by Inhibiting the K + Channel (Kir4.1) in the Distal Convoluted Tubule
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Hypertension Vol. 72, No. 2 ( 2018-08), p. 361-369
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 72, No. 2 ( 2018-08), p. 361-369
    Abstract: Stimulation 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). Immunohistochemical studies demonstrated that BK2R was highly expressed in both apical and lateral membrane of Kir4.1-positive tubules, such as DCT. Patch-clamp experiments demonstrated that BK inhibited the basolateral 40-pS K + channel (a Kir4.1/5.1 heterotetramer) in the DCT, and this effect was blocked by BK2R antagonist but not by BK1R (BK B1 receptor) antagonist. Whole-cell recordings also demonstrated that BK decreased the basolateral K + conductance of the DCT and depolarized the membrane. Renal clearance experiments showed that BK increased urinary Na + and K + excretion. However, the BK-induced natriuretic effect was completely abolished in KS-Kir4.1 KO (kidney-specific conditional Kir4.1 knockout) mice, suggesting that Kir4.1 activity is required for BK-induced natriuresis. The continuous infusion of BK with osmotic pump for 3 days decreased the basolateral K + conductance and the negativity of the DCT membrane. Western blot showed that infusion of BK decreased the expression of total NCC and phosphorylated NCC. Renal clearance experiments demonstrated that thiazide-induced natriuresis was blunted in the mice receiving BK infusion, suggesting that BK inhibited NCC function. Consequently, mice receiving BK infusion for 3 days were hypokalemic. We conclude that stimulation of BK2R inhibits NCC activity, increases urinary K + excretion, and causes mice hypokalemia and that Kir4.1 is required for BK2R-mediated stimulation of urinary Na + and K + excretion.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.118.11070
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
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  • 3
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    Kir5.1 is essential for the effect of dietary potassium intake on the basolateral K channels and Na‐Cl cotransporter (NCC) in the distal convoluted tubule (DCT)
    Wiley ; 2019
    In:  The FASEB Journal Vol. 33, No. S1 ( 2019-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 33, No. S1 ( 2019-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v33.S1
    DOI: 10.1096/fasebj.2019.33.1_supplement.862.1
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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  • 4
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    Role of WNK4 and kidney-specific WNK1 in mediating the effect of high dietary K + intake on ROMK channel in the distal convoluted tubule
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Renal Physiology Vol. 315, No. 2 ( 2018-08-01), p. F223-F230
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 315, No. 2 ( 2018-08-01), p. F223-F230
    Abstract: With-no-lysine kinase 4 (WNK4) and kidney-specific (KS)-WNK1 regulate ROMK (Kir1.1) channels in a variety of cell models. We now explore the role of WNK4 and KS-WNK1 in regulating ROMK in the native distal convoluted tubule (DCT)/connecting tubule (CNT) by measuring tertiapin-Q (TPNQ; ROMK inhibitor)-sensitive K + currents with whole cell recording. TPNQ-sensitive K + currents in DCT2/CNT of KS- WNK1 −/− and WNK4 −/− mice were significantly smaller than that of WT mice. In contrast, the basolateral K + channels (a Kir4.1/5.1 heterotetramer) in the DCT were not inhibited. Moreover, WNK4 −/− mice were hypokalemic, while KS- WNK1 −/− mice had normal plasma K + levels. High K + (HK) intake significantly increased TPNQ-sensitive K + currents in DCT2/CNT of WT and WNK4 −/− mice but not in KS- WNK1 −/− mice. However, TPNQ-sensitive K + currents in the cortical collecting duct (CCD) were normal not only under control conditions but also significantly increased in response to HK in KS- WNK1 −/− mice. This suggests that the deletion of KS-WNK1-induced inhibition of ROMK occurs only in the DCT2/CNT. Renal clearance study further demonstrated that the deletion of KS-WNK1 did not affect the renal ability of K + excretion under control conditions and during increasing K + intake. Also, HK intake did not cause hyperkalemia in KS- WNK1 −/− mice. We conclude that KS-WNK1 but not WNK4 is required for HK intake-induced stimulation of ROMK activity in DCT2/CNT. However, KS-WNK1 is not essential for HK-induced stimulation of ROMK in the CCD, and the lack of KS-WNK1 does not affect net renal K + excretion.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00050.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
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  • 5
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    Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of the American Society of Nephrology Vol. 31, No. 6 ( 2020-6), p. 1226-1242
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 6 ( 2020-6), p. 1226-1242
    Abstract: The potassium channel Kir4.1 forms the Kir4.1/Kir5.1 heterotetramer in the basolateral membrane of the distal convoluted tubule (DCT) and plays an important role in regulating the thiazide-sensitive NaCl cotransporter (NCC). Deletion of the ubiquitin ligase Nedd4-2 has been shown to increase the expression of NCC and to cause salt-sensitive hypertension. The authors demonstrated that kidney-specific deletion of Nedd4-2 in mice also stimulates Kir4.1/Kir5.1 activity in the DCT and hyperpolarizes the DCT membrane. They also found that NCC activity/expression is largely inhibited in double-knockout mice deficient in both Kir4.1 and Nedd4-2 and that NCC activity/expression is higher in these double-knockout mice compared with mice lacking only Kir4.1. These findings suggest that Nedd4-2 regulates NCC expression through modulation of basolateral Kir4.1/Kir5.1 activity and through Kir4.1-independent regulation of NCC retrieval. Background The potassium channel Kir4.1 forms the Kir4.1/Kir5.1 heterotetramer in the basolateral membrane of the distal convoluted tubule (DCT) and plays an important role in the regulation of the thiazide-sensitive NaCl cotransporter (NCC). Kidney-specific deletion of the ubiquitin ligase Nedd4-2 increases expression of NCC, and coexpression of Nedd4-2 inhibits Kir4.1/Kir5.1 in vitro . Whether Nedd4-2 regulates NCC expression in part by regulating Kir4.1/Kir5.1 channel activity in the DCT is unknown. Methods We used electrophysiology studies, immunoblotting, immunostaining, and renal clearance to examine Kir4.1/Kir5.1 activity in the DCT and NCC expression/activity in wild-type mice and mice with kidney-specific knockout of Nedd4-2, Kir4.1, or both. Results Deletion of Nedd4-2 increased the activity/expression of Kir4.1 in the DCT and also, hyperpolarized the DCT membrane. Expression of phosphorylated NCC/total NCC and thiazide-induced natriuresis were significantly increased in the Nedd4-2 knockout mice, but these mice were normokalemic. Double-knockout mice lacking both Kir4.1/Kir5.1 and Nedd4-2 in the kidney exhibited increased expression of the epithelial sodium channel α -subunit, largely abolished basolateral potassium ion conductance (to a degree similar to that of kidney-specific Kir4.1 knockout mice), and depolarization of the DCT membrane. Compared with wild-type mice, the double-knockout mice displayed inhibited expression of phosphorylated NCC and total NCC and had significantly blunted thiazide-induced natriuresis as well as renal potassium wasting and hypokalemia. However, NCC expression/activity was higher in the double-knockout mice than in Kir4.1 knockout mice. Conclusions Nedd4-2 regulates Kir4.1/Kir5.1 expression/activity in the DCT and modulates NCC expression by Kir4.1-dependent and Kir4.1-independent mechanisms. Basolateral Kir4.1/Kir5.1 activity in the DCT partially accounts for the stimulation of NCC activity/expression induced by deletion of Nedd4-2.
    Type of Medium: Online Resource
    ISSN: 1046-6673 , 1533-3450
    URL: Article
    DOI: 10.1681/ASN.2019090923
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
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  • 6
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    Emerging role of antidiabetic drugs in cardiorenal protection
    Frontiers Media SA ; 2024
    In:  Frontiers in Pharmacology Vol. 15 ( 2024-2-6)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 15 ( 2024-2-6)
    Abstract: The global prevalence of diabetes mellitus (DM) has led to widespread multi-system damage, especially in cardiovascular and renal functions, heightening morbidity and mortality. Emerging antidiabetic drugs sodium-glucose cotransporter 2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1RAs), and dipeptidyl peptidase-4 inhibitors (DPP-4i) have demonstrated efficacy in preserving cardiac and renal function, both in type 2 diabetic and non-diabetic individuals. To understand the exact impact of these drugs on cardiorenal protection and underlying mechanisms, we conducted a comprehensive review of recent large-scale clinical trials and basic research focusing on SGLT2i, GLP-1RAs, and DPP-4i. Accumulating evidence highlights the diverse mechanisms including glucose-dependent and independent pathways, and revealing their potential cardiorenal protection in diabetic and non-diabetic cardiorenal disease. This review provides critical insights into the cardiorenal protective effects of SGLT2i, GLP-1RAs, and DPP-4i and underscores the importance of these medications in mitigating the progression of cardiovascular and renal complications, and their broader clinical implications beyond glycemic management.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2024.1349069
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2024
    detail.hit.zdb_id: 2587355-6
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  • 7
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    Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel
    Elsevier BV ; 2018
    In:  Kidney International Vol. 93, No. 4 ( 2018-04), p. 893-902
    Details
    In: Kidney International, Elsevier BV, Vol. 93, No. 4 ( 2018-04), p. 893-902
    Type of Medium: Online Resource
    ISSN: 0085-2538
    URL: Article
    DOI: 10.1016/j.kint.2017.10.023
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2007940-0
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  • 8
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    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
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Renal Physiology Vol. 320, No. 5 ( 2021-05-01), p. F883-F896
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 320, No. 5 ( 2021-05-01), p. F883-F896
    Abstract: 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 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 Kir4.1, NCC, ENaC, and renal K + excretion. Immunoblot analysis showed that HS diet decreased the expression of Kir4.1, Ca 2+ -activated large-conductance K + channel subunit-α (BKα), ENaCβ, ENaCγ, total NCC, and phospho-NCC (at Thr 53 ) in floxed neural precursor cell expressed developmentally downregulated gene 4-like ( Nedd4l fl/fl ) mice, whereas these effects were absent in kidney-specific Nedd4-2 knockout (Ks-Nedd4-2 KO) mice. Renal clearance experiments also demonstrated that Nedd4-2 deletion abolished the inhibitory effect of HS diet on hydrochlorothiazide-induced natriuresis. Patch-clamp experiments showed that neither HS diet nor low-salt diet had an effect on Kir4.1/Kir5.1 currents of the distal convoluted tubule in Nedd4-2-deficient mice, whereas we confirmed that HS diet inhibited and low-salt diet increased Kir4.1/Kir5.1 activity in Nedd4l flox/flox mice. Nedd4-2 deletion increased ENaC currents in the ASDN, and this increase was more robust in the cortical collecting duct than in the distal convoluted tubule. Also, HS-induced inhibition of ENaC currents in the ASDN was absent in Nedd4-2-deficient mice. Renal clearance experiments showed that HS intake for 2 wk increased the basal level of renal K + excretion and caused hypokalemia in Ks-Nedd4-2-KO mice but not in Nedd4l flox/flox mice. In contrast, plasma Na + concentrations were similar in Nedd4l flox/flox and Ks-Nedd4-2 KO mice on HS diet. We conclude that Nedd4-2 plays an important role in mediating the inhibitory effect of HS diet on Kir4.1, ENaC, and NCC and is essential for maintaining normal renal K + excretion and plasma K + ranges during long-term HS diet. NEW & NOTEWORTHY The present study suggests that Nedd4-2 is involved in mediating the inhibitory effect of high salt (HS) diet on Kir4.1/kir5.1 in the distal convoluted tubule, NaCl cotransporter function, and epithelial Na + channel activity and that Nedd4-2 plays an essential role in maintaining K + homeostasis in response to a long-term HS diet. This suggests the possibility that HS intake could lead to hypokalemia in subjects lacking proper Nedd4-2 E3 ubiquitin ligase activity in aldosterone-sensitive distal nephron.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00555.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
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  • 9
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    Kir5.1 regulates Nedd4-2-mediated ubiquitination of Kir4.1 in distal nephron
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Renal Physiology Vol. 315, No. 4 ( 2018-10-01), p. F986-F996
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 315, No. 4 ( 2018-10-01), p. F986-F996
    Abstract: 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). Kir5.1 contains a phosphothreonine motif at its COOH terminus (AA249–252). Coimmunoprecipitation showed that Nedd4-2 was associated with Kir5.1 in HEK293 cells cotransfected with Kir5.1 or Kir4.1/Kir5.1. GST pull-down further confirmed the association between Nedd4-2 and Kir5.1. Ubiquitination assay showed that Nedd4-2 increased the ubiquitination of Kir4.1/Kir5.1 heterotetramer in the cells cotransfected with Kir4.1/Kir5.1, but it has no effect on Kir4.1 or Kir5.1 alone. Patch-clamp and Western blot also demonstrated that coexpression of Nedd4-2 but not Nedd4-1 decreased K currents and Kir4.1 expression in the cells cotransfected with Kir4.1 and Kir5.1. In contrast, Nedd4-2 fails to inhibit Kir4.1 in the absence of Kir5.1 or in the cells transfected with the inactivated form of Nedd4-2 (Nedd4-2C821A). Moreover, the mutation of TPVT motif in the COOH terminus of Kir5.1 largely abolished the association of Nedd4-2 with Kir5.1 and abolished the inhibitory effect of Nedd4-2 on K currents in HEK293 cells transfected with Kir4.1 and Kir5.1 mutant (Kir5.1T249A). Finally, the basolateral K conductance in the DCT and Kir4.1 expression is significantly increased in the kidney-specific Nedd4-2 knockout or in Kir5.1 knockout mice in comparison to their corresponding wild-type littermates. We conclude that Nedd4-2 binds to Kir5.1 at the phosphothreonine motif of the COOH terminus, and the association of Nedd4-2 with Kir5.1 facilitates the ubiquitination of Kir4.1, thereby regulating its plasma expression in the DCT.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00059.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2018
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  • 10
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    Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake–Induced Modulation of Na-Cl Cotransporter
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of the American Society of Nephrology Vol. 30, No. 2 ( 2019-2), p. 216-227
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 2 ( 2019-2), p. 216-227
    Abstract: Considerable evidence indicates that basolateral inwardly rectifying potassium channel Kir4.1/Kir5.1 is essential for membrane transport in the distal convoluted tubule (DCT), and that dietary sodium and potassium are important in regulating activity of the thiazide-sensitive Na-Cl cotransporter (NCC). In mouse studies, the authors found that stimulation of NCC induced by sodium restriction was associated with increasing Kir4.1/Kir5.1 activity in the DCT and membrane hyperpolarization; NCC inhibition induced by high sodium intake was associated with decreasing Kir4.1/Kir5.1 activity in the DCT and membrane depolarization. In kidney-specific Kir4.1 knockout mice, the effect of dietary sodium on NCC activity was largely abolished, as were its effects on DCT membrane conductance and potential. The findings indicate that Kir4.1/Kir5.1 is essential for mediating dietary sodium intake–induced modulation of NCC function. Background 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/Kir5.1 (a heterotetramer of Kir4.1/Kir5.1) in the DCT is essential for mediating the effect of dietary sodium intake on NCC activity is unknown. Methods We used electrophysiology, renal clearance techniques, and immunoblotting to examine effects of Kir4.1/Kir5.1 in the DCT and NCC in wild-type and kidney-specific Kir4.1 knockout mice. Results Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K + conductance, and hyperpolarized the membrane. Conversely, high sodium intake inhibited the potassium channel, decreased basolateral K + currents, and depolarized the membrane. Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. In contrast, dietary sodium intake did not affect NCC activity in knockout mice. Further, Kir4.1 deletion not only abolished basolateral K + conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K + conductance and hyperpolarization. Finally, dietary sodium intake did not alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice. Conclusions Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC.
    Type of Medium: Online Resource
    ISSN: 1046-6673 , 1533-3450
    URL: Article
    DOI: 10.1681/ASN.2018080799
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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