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  • 1
    Online Resource
    Online Resource
    17β-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1
    American Physiological Society ; 2012
    In:  American Journal of Physiology-Renal Physiology Vol. 302, No. 3 ( 2012-02-01), p. F358-F368
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 302, No. 3 ( 2012-02-01), p. F358-F368
    Abstract: Steroid hormones such as 17β-estradiol (E2) are known to modulate ion transporter expression in the kidney through classic intracellular receptors. Steroid hormones are also known to cause rapid nongenomic responses in a variety of nonrenal tissues. However, little is known about renal short-term effects of steroid hormones. Here, we studied the acute actions of E2 on intracellular Ca 2+ signaling in isolated distal convoluted tubules (DCT2), connecting tubules (CNT), and initial cortical collecting ducts (iCCD) by fluo 4 fluorometry. Physiological concentrations of E2 induced transient increases in intracellular Ca 2+ concentration ([Ca 2+ ] i ) in a subpopulation of cells. The [Ca 2+ ] i increases required extracellular Ca 2+ and were inhibited by Gd 3+ . Strikingly, the classic E2 receptor antagonist ICI 182,780 also increased [Ca 2+ ] i , which is inconsistent with the activation of classic E2 receptors. G protein-coupled estrogen receptor 1 (GPER1 or GPR30) was detected in microdissected DCT2/CNT/iCCD by RT-PCR. Stimulation with the specific GPER1 agonist G-1 induced similar [Ca 2+ ] i increases as E2, and in tubules from GPER1 knockout mice, E2, G-1, and ICI 182,780 failed to induce [Ca 2+ ] i elevations. The intercalated cells showed both E2-induced concanamycin-sensitive H + -ATPase activity by BCECF fluorometry and the E2-mediated [Ca 2+ ] i increment. We propose that E2 via GPER1 evokes [Ca 2+ ] i transients and increases H + -ATPase activity in intercalated cells in mouse DCT2/CNT/iCCD.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00343.2011
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1477287-5
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  • 2
    Online Resource
    Online Resource
    Assessment of the Effect of 24-Hour Aldosterone Administration on Protein Abundance in Fluorescence-Sorted Mouse Distal Renal Tubules by Mass Spectrometry
    S. Karger AG ; 2013
    In:  Nephron Physiology Vol. 121, No. 3-4 ( 2013-2-14), p. p9-p15
    Details
    In: Nephron Physiology, S. Karger AG, Vol. 121, No. 3-4 ( 2013-2-14), p. p9-p15
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Aldosterone exerts multiple long-term effects on the distal renal tubules. The aim of this study was to establish a method for identifying proteins in these tubules that change in abundance by only 24-hour aldosterone administration. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Mice endogenously expressing green fluorescent protein (eGFP) in the connecting tubule and cortical collecting ducts were treated with a subcutaneous injection of 2.0 mg/kg aldosterone or vehicle (n = 5), and sacrificed 24 h later. Suspensions of single cells were obtained enzymatically, and eGFP-positive cells were isolated by fluorescence-activated cell sorting (FACS). Samples of 100 µg of proteins were digested with trypsin and labeled with 8-plex isobaric tags for relative and absolute quantitation reagents and processed for liquid chromatography-tandem mass spectrometry (LC-MS/MS). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 FACS yielded 1.4 million cells per mouse. The LC-MS/MS spectra were matched to peptides by the SEQUEST search algorithm, which identified 3,002 peptides corresponding to 506 unique proteins, of which 20 significantly changed abundance 24 h after aldosterone injection. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 We find the method suitable and useful for studying hormonal effects on protein abundance in distal tubular segments.
    Type of Medium: Online Resource
    ISSN: 1660-2137
    URL: Article
    DOI: 10.1159/000346832
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2013
    detail.hit.zdb_id: 2098340-2
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  • 3
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    Identification of proteins regulated by 24‐hour aldosterone treatment in late distal convoluted tubules, connecting tubules and initial cortical collecting ducts
    Wiley ; 2012
    In:  The FASEB Journal Vol. 26, No. S1 ( 2012-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 26, No. S1 ( 2012-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v26.S1
    DOI: 10.1096/fasebj.26.1_supplement.885.9
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 4
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    Online Resource
    Isolation of single cells from murine late distal convoluted tubules and connecting tubules
    Wiley ; 2011
    In:  The FASEB Journal Vol. 25, No. S1 ( 2011-04)
    Details
    In: The FASEB Journal, Wiley, Vol. 25, No. S1 ( 2011-04)
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v25.S1
    DOI: 10.1096/fasebj.25.1_supplement.863.7
    Language: English
    Publisher: Wiley
    Publication Date: 2011
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 5
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    Online Resource
    [Ca2+] Oscillations and IL-6 Release Induced by α-Hemolysin from Escherichia coli Require P2 Receptor Activation in Renal Epithelia
    Elsevier BV ; 2015
    In:  Journal of Biological Chemistry Vol. 290, No. 23 ( 2015-06), p. 14776-14784
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 290, No. 23 ( 2015-06), p. 14776-14784
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M115.639526
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
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  • 6
    Online Resource
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    Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Renal Physiology Vol. 291, No. 5 ( 2006-11), p. F1021-F1032
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 291, No. 5 ( 2006-11), p. F1021-F1032
    Abstract: The renin-angiotensin system is well known to be involved in the pathophysiological changes in renal function after obstruction of the ureter. Previously, we demonstrated that bilateral ureteral obstruction (BUO) is associated with dramatic changes in the expression of both renal sodium transporters and aquaporin water channels (AQPs). We now examined the effects of the AT 1 -receptor antagonist candesartan on the dysregulation of AQPs and key renal sodium transporters in rats subjected to 24-h BUO and followed 2 days after release of BUO (BUO-2R). Consistent with previous observations, BUO-2R resulted in a significantly decreased expression of AQP1, -2, and -3 compared with control rats. Concomitantly, the rats developed polyuria and reduced urine osmolality. Moreover, expression of the type 2 Na-phosphate cotransporter (NaPi-2) and type 1 bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) was markedly reduced, consistent with postobstructive natriuresis. Candesartan treatment from the onset of obstruction attenuated the reduction in GFR (3.1 ± 0.4 vs. 1.7 ± 0.3 ml·min −1 ·kg −1 ) and partially prevented the reduction in the expression of AQP2 (66 ± 21 vs. 13 ± 2%, n = 7; P 〈 0.05), NaPi-2 (84 ± 6 vs. 57 ± 10%, n = 7; P 〈 0.05), and NKCC2 (89 ± 12 vs. 46% ± 11, n = 7; P 〈 0.05). Consistent with this, candesartan treatment attenuated the increase in urine output (58 ± 4 vs. 97 ± 5 μl·min −1 ·kg −1 , n = 7; P 〈 0.01) and the reduction in sodium reabsorption (433 ± 62 vs. 233 ± 45 μmol·min −1 ·kg −1 , n = 7; P 〈 0.05) normally found in rats subjected to BUO. Moreover, candesartan treatment attenuated induction of cyclooxygenase 2 (COX-2) expression in the inner medulla, suggesting that COX-2 induction in response to obstruction is regulated by ANG II. In conclusion, candesartan prevents dysregulation of AQP2, sodium transporters, and development of polyuria seen in BUO. This strongly supports the view that candesartan protects kidney function in response to urinary tract obstruction.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00387.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477287-5
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  • 7
    Online Resource
    Online Resource
    Basolateral P2X receptors mediate inhibition of NaCl transport in mouse medullary thick ascending limb (mTAL)
    American Physiological Society ; 2012
    In:  American Journal of Physiology-Renal Physiology Vol. 302, No. 4 ( 2012-02-15), p. F487-F494
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 302, No. 4 ( 2012-02-15), p. F487-F494
    Abstract: Extracellular nucleotides regulate epithelial transport via luminal and basolateral P2 receptors. Renal epithelia express multiple P2 receptors, which mediate significant inhibition of solute absorption. Recently, we identified several P2 receptors in the medullary thick ascending limb (mTAL) including luminal and basolateral P2Y 2 receptors (Jensen ME, Odgaard E, Christensen MH, Praetorius HA, Leipziger J. J Am Soc Nephrol 18: 2062–2070, 2007). In addition, we found evidence for a basolateral P2X receptor. Here, we investigate the effect of basolateral ATP on NaCl absorption in isolated, perfused mouse mTALs using the electrical measurement of equivalent short-circuit current ( I′ sc ). Nonstimulated mTALs transported at a rate of 1,197 ± 104 μA/cm 2 ( n = 10), which was completely blockable with luminal furosemide (100 μM). Basolateral ATP (100 μM) acutely (1 min) and reversibly reduced the absorptive I′ sc . After 2 min, the reduction amounted to 24.4 ± 4.0% ( n = 10). The nonselective P2 receptor antagonist suramin blocked the effect. P2Y receptors were found not to be involved in this effect. The P2X receptor agonist 2-methylthio ATP mimicked the ATP effect, and the P2X receptor antagonist periodate-oxidized ATP blocked it. In P2X 7 −/− mice, the ATP effect remained unaltered. In contrast, in P2X 4 −/− mice the ATP-induced inhibition of transport was reduced. A comprehensive molecular search identified P2X 4 , P2X 5 , and P2X 1 receptor subunit mRNA in isolated mouse mTALs. These data define that basolateral ATP exerts a significant inhibition of Na + absorption in mouse mTAL. Pharmacological, molecular, and knockout mouse data identify a role for the P2X 4 receptor. We suggest that other P2X subunits like P2X 5 are part of the P2X receptor complex. These data provide the novel perspective that an ionotropic receptor and thus a nonselective cation channel causes transport inhibition in an intact renal epithelium.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00570.2011
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
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  • 8
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    Online Resource
    Vasopressin-independent targeting of aquaporin-2 by selective E-prostanoid receptor agonists alleviates nephrogenic diabetes insipidus
    Proceedings of the National Academy of Sciences ; 2011
    In:  Proceedings of the National Academy of Sciences Vol. 108, No. 31 ( 2011-08-02), p. 12949-12954
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 108, No. 31 ( 2011-08-02), p. 12949-12954
    Abstract: In the kidney, the actions of vasopressin on its type-2 receptor (V2R) induce increased water reabsorption alongside polyphosphorylation and membrane targeting of the water channel aquaporin-2 (AQP2). Loss-of-function mutations in the V2R cause X-linked nephrogenic diabetes insipidus. Treatment of this condition would require bypassing the V2R to increase AQP2 membrane targeting, but currently no specific pharmacological therapy is available. The present study examined specific E-prostanoid receptors for this purpose. In vitro, prostaglandin E2 (PGE2) and selective agonists for the E-prostanoid receptors EP2 (butaprost) or EP4 (CAY10580) all increased trafficking and ser-264 phosphorylation of AQP2 in Madin-Darby canine kidney cells. Only PGE2 and butaprost increased cAMP and ser-269 phosphorylation of AQP2. Ex vivo, PGE2, butaprost, or CAY10580 increased AQP2 phosphorylation in isolated cortical tubules, whereas PGE2 and butaprost selectively increased AQP2 membrane accumulation in kidney slices. In vivo, a V2R antagonist caused a severe urinary concentrating defect in rats, which was greatly alleviated by treatment with butaprost. In conclusion, EP2 and EP4 agonists increase AQP2 phosphorylation and trafficking, likely through different signaling pathways. Furthermore, EP2 selective agonists can partially compensate for a nonfunctional V2R, providing a rationale for new treatment strategies for hereditary nephrogenic diabetes insipidus.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1104691108
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2011
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 9
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    Furosemide-induced urinary acidification is caused by pronounced H + secretion in the thick ascending limb
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Renal Physiology Vol. 309, No. 2 ( 2015-07-15), p. F146-F153
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 309, No. 2 ( 2015-07-15), p. F146-F153
    Abstract: The loop diuretic furosemide inhibits NaCl reabsorption in the thick ascending limb (TAL). In addition, furosemide acidifies the urine, which is traditionally explained by increased Na + loading to the distal tubule causing an activation of H + secretion via H + -ATPase in α-intercalated cells. The inability to acidify urine in response to furosemide serves to diagnose distal renal tubular acidosis (dysfunction of α-intercalated cells). Since the TAL is important for acid/base regulation, we speculated that it is involved in furosemide-induced urinary acidification. Luminal furosemide (100 μM) caused major, stable, and reversible intracellular alkalization (7.27 ± 0.06 to 7.6 ± 0.04) in isolated perfused murine medullary TAL and pronounced H + secretion. This H + secretion was fully inhibited with luminal amiloride (1 mM) and the Na + /H + exchanger (NHE)3-specific antagonist #4167 (1 μM). Moreover, furosemide triggered a substantial drop of intracellular Na + concentration in the medullary TAL. These results suggest that the furosemide-induced H + secretion is a consequence of a drop in intracellular Na + concentration, increasing the driving force for NHE3. Intriguingly, in whole animal experiments, furosemide-induced urinary acidification and net acid excretion were markedly reduced by specific NHE3 inhibition. Furthermore, the furosemide-induced urinary acidification was partially preserved during epithelial Na + channel inhibition with benzamil. These results provide new insights in the mechanism of furosemide-induced urinary acidification and emphasize the role of the TAL in renal acid/base handling.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00154.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
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  • 10
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    Interaction Between Na + /K + -Pump and Na + /Ca 2+ -Exchanger Modulates Intercellular Communication
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Research Vol. 100, No. 7 ( 2007-04-13), p. 1026-1035
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 7 ( 2007-04-13), p. 1026-1035
    Abstract: Ouabain, a specific inhibitor of the Na + /K + -pump, has previously been shown to interfere with intercellular communication. Here we test the hypothesis that the communication between vascular smooth muscle cells is regulated through an interaction between the Na + /K + -pump and the Na + /Ca 2+ -exchanger leading to an increase in the intracellular calcium concentration ([Ca 2+ ] i ) in discrete areas near the plasma membrane. [Ca 2+ ] i in smooth muscle cells was imaged in cultured rat aortic smooth muscle cell pairs (A7r5) and in rat mesenteric small artery segments simultaneously with force. In A7r5 coupling between cells was estimated by measuring membrane capacitance. Smooth muscle cells were uncoupled when the Na + /K + -pump was inhibited either by a low concentration of ouabain, which also caused a localized increase of [Ca 2+ ] i near the membrane, or by ATP depletion. Reduction of Na + /K + -pump activity by removal of extracellular potassium ([K + ] o ) also uncoupled cells, but only after inhibition of K ATP channels. Inhibition of the Na + /Ca 2+ -exchange activity by SEA0400 or by a reduction of the equilibrium potential (making it more negative) also uncoupled the cells. Depletion of intracellular Na + and clamping of [Ca 2+ ] i at low concentrations prevented the uncoupling. The experiments suggest that the Na + /K + -pump may affect gap junction conductivity via localized changes in [Ca 2+ ] i through modulation of Na + /Ca 2+ -exchanger activity.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000262659.09293.56
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1467838-X
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