GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Identification of Two Nuclear Factor of Activated T-cells (NFAT)-response Elements in the 5′-Upstream Regulatory Region of the ET-1 Promoter
    Elsevier BV ; 2010
    In:  Journal of Biological Chemistry Vol. 285, No. 37 ( 2010-09), p. 28520-28528
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 285, No. 37 ( 2010-09), p. 28520-28528
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M110.153189
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Calcium regulation of endothelin-1 synthesis in rat inner medullary collecting duct
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Renal Physiology Vol. 293, No. 2 ( 2007-08), p. F601-F606
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 293, No. 2 ( 2007-08), p. F601-F606
    Abstract: Collecting duct-derived endothelin-1 (ET-1) reduces blood pressure and inhibits Na and water reabsorption. Collecting duct ET-1 production is increased by volume expansion; however, the mechanism by which this occurs is unknown. We hypothesized that intracellular calcium, which is likely to be increased by volume expansion, regulates collecting duct ET-1 synthesis. Rat inner medullary collecting ducts (IMCD) were studied in primary culture. ET-1 release was decreased by 50–70% after chelation of intracellular calcium (BAPTA) or inhibition of CaM (W7) or CaMK (KN-93). These agents reduced ET-1 mRNA to a similar degree. CaM inhibition did not affect ET-1 mRNA stability. Transfection of IMCD with rat ET-1 promoter-luciferase constructs revealed maximal activity within 1.7 kb 5′ to the transcription start site; 5, 20, 35, and 90% of this activity were in the 0.08-, 0.37-, 1.0-, and 3.0-kb promoter regions, respectively. W7 markedly inhibited activity of the 3.0-kb but not 0.37- or 1.0-kb promoter regions. In contrast, W7 did not affect ET-1 release by rat aortic endothelial cells. Furthermore, transfected endothelial cells had maximal activity in the 0.37-kb region (as compared with the 1.7- and 3.0-kb regions), whereas W-7 had no effect on the activity of any of these promoter regions. In summary, IMCD ET-1 synthesis is regulated by calcium/CaM/CaMK-dependent pathways. The calcium/CaM-sensitive pathway is active in IMCD, but not endothelial cells. This suggests that IMCD-specific enhancer elements exist within the ET-1 promoter that confer unique calcium responsiveness.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00085.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477287-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Smooth muscle specific disruption of the endothelin-A receptor in mice reduces arterial pressure, and vascular reactivity and affects vascular development
    Elsevier BV ; 2014
    In:  Life Sciences Vol. 118, No. 2 ( 2014-11), p. 238-243
    Details
    In: Life Sciences, Elsevier BV, Vol. 118, No. 2 ( 2014-11), p. 238-243
    Type of Medium: Online Resource
    ISSN: 0024-3205
    URL: Article
    DOI: 10.1016/j.lfs.2013.12.209
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2013911-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Abstract 014: Collecting Duct Specific Deletion of the (Pro)renin Receptor Modulates ENaC Expression
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 68, No. suppl_1 ( 2016-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 68, No. suppl_1 ( 2016-09)
    Abstract: The renal tubular (pro)renin receptor (PRR) has been shown to modulate water balance, blood pressure and Na + homeostasis. We recently reported that inducible nephron wide deletion of the PRR results in Na + wasting, reduced epithelial Na + channel (ENaC) expression in the kidney and attenuated hypertensive response to angiotensin-II (Ang-II) infusion. In this study, we examined the effects of PRR deletion in collecting duct (CD) specific mouse models targeting either the principal cells (PC) or intercalated cells (IC). PC-specific PRR knockout (KO) mice were obtained by crossing floxed PRR mice with mice harboring AQP-2 Cre recombinase. Compared to floxed mice, PC specific KO PRR mice had no differences in PRR immunostaining but had 50% reduction in PRR mRNA in micro-dissected cortical CDs. No differences in blood pressure were observed between the two groups at baseline or following Ang-II infusion at 600 ng/kg/min. Similarly, plasma renin concentration and renal expression of ENaC protein isoforms were comparable between the two groups. To achieve IC-specific PRR deletion, floxed PRR mice were bred with mice expressing B-1 Cre recombinase. Compared to floxed controls, IC-specific PRR KO mice were smaller (KO body weight: 5.9 ± 1.3 g vs controls: 11.1± 1.2 g) and did not survive beyond 30 days after birth. IC-specific PRR KO mice also demonstrated marked reduction in renal medullary PRR immunostaining along with decreased renal expression of ENaC-α protein (50% reduction compared to controls), similar to the findings in nephron wide deletion of PRR. Taken together, these findings suggest that IC specific deletion of PRR but not PC-specific deletion modulates renal ENaC expression. Further studies evaluating ENaC activity in isolated cortical CDs from PC and IC specific PRR KO mice will help delineate the functional role of CD PRR in Na + homeostasis.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.68.suppl_1.014
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Renal Collecting Duct NOS1 Maintains Fluid–Electrolyte Homeostasis and Blood Pressure
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. 1 ( 2013-07), p. 91-98
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. 1 ( 2013-07), p. 91-98
    Abstract: Nitric oxide is a pronatriuretic and prodiuretic factor. The highest renal NO synthase (NOS) activity is found in the inner medullary collecting duct. The collecting duct (CD) is the site of daily fine-tune regulation of sodium balance, and led us to hypothesize that a CD-specific deletion of NOS1 would result in an impaired ability to excrete a sodium load leading to a salt-sensitive blood pressure phenotype. We bred AQP2-CRE mice with NOS1 floxed mice to produce flox control and CD-specific NOS1 knockout (CDNOS1KO) littermates. CDs from CDNOS1KO mice produced 75% less nitrite, and urinary nitrite+nitrate (NOx) excretion was significantly blunted in the knockout genotype. When challenged with high dietary sodium, CDNOS1KO mice showed significantly reduced urine output, sodium, chloride, and NOx excretion, and increased mean arterial pressure relative to flox control mice. In humans, urinary NOx is a newly identified biomarker for the progression of hypertension. These findings reveal that NOS1 in the CD is critical in the regulation of fluid–electrolyte balance, and this new genetic model of CD NOS1 gene deletion will be a valuable tool to study salt-dependent blood pressure mechanisms.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.113.01291
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Altered collecting duct adenylyl cyclase content in collecting duct endothelin-1 knockout mice
    Springer Science and Business Media LLC ; 2007
    In:  BMC Nephrology Vol. 8, No. 1 ( 2007-12)
    Details
    In: BMC Nephrology, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2007-12)
    Abstract: Endothelin-1 (ET-1) inhibition of vasopressin (AVP)-stimulated water reabsorption by the inner medullary collecting duct (IMCD) is associated with reduced cAMP accumulation. To determine the effect of ET-1 deficiency, AVP-stimulated cAMP responsiveness was assessed in IMCD from mice with collecting duct-specific deletion of ET-1 (CD ET-1 KO) and from control animals. Methods Cyclic AMP production, adenylyl cyclase (AC) mRNA, and AC protein were measured in acutely isolated IMCD. Results CD ET-1 KO IMCD had enhanced AVP-stimulated cAMP accumulation. Inhibition of calcium-stimulated AC using BAPTA did not prevent enhanced AVP responsiveness in CD ET-1 KO IMCD. Factors known to be modified by ET-1, including nitric oxide, cyclooxygenase metabolites, and superoxide did not affect the increased AVP responsiveness of CD ET-1 KO IMCD. Differential V2 receptor or G-protein activity was not involved since CD ET-1 KO IMCD had increased cAMP accumulation in response to forskolin and/or cholera toxin. CD ET-1 KO did not affect mRNA or protein levels of AC3, one of the major known collecting duct AC isoforms. However, the other known major collecting duct AC isoform (AC5/6) did have increased protein levels in CD ET-1 KO IMCD, although AC5 (weak signal) and 6 mRNA levels were unchanged. Conclusion ET-1 deficiency increases IMCD AC5/6 content, an effect that may synergize with acute ET-1 inhibition of AVP-stimulated cAMP accumulation.
    Type of Medium: Online Resource
    ISSN: 1471-2369
    URL: Article
    DOI: 10.1186/1471-2369-8-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2007
    detail.hit.zdb_id: 2041348-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Disruption of the endothelin A receptor in the nephron causes mild fluid volume expansion
    Springer Science and Business Media LLC ; 2012
    In:  BMC Nephrology Vol. 13, No. 1 ( 2012-12)
    Details
    In: BMC Nephrology, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2012-12)
    Abstract: Endothelin, via endothelin A receptors (ETA), exerts multiple pathologic effects that contribute to disease pathogenesis throughout the body. ETA antagonists ameliorate many experimental diseases and have been extensively utilized in clinical trials. The utility of ETA blockers has been greatly limited, however, by fluid retention, sometimes leading to heart failure or death. To begin to examine this issue, the effect of genetic disruption of ETA in the nephron on blood pressure and salt handling was determined. Methods Mice were generated with doxycycline-inducible nephron-specific ETA deletion using Pax8-rtTA and LC-1 transgenes on the background of homozygous loxP-flanked ETA alleles. Arterial pressure, Na metabolism and measures of body fluid volume status (hematocrit and impedance plethysmography) were assessed. Results Absence of nephron ETA did not alter arterial pressure whether mice were ingesting a normal or high Na diet. Nephron ETA disruption did not detectably affect 24 hr Na excretion or urine volume regardless of Na intake. However, mice with nephron ETA knockout that were fed a high Na diet had mild fluid retention as evidenced by an increase in body weight and a fall in hematocrit. Conclusions Genetic deletion of nephron ETA causes very modest fluid retention that does not alter arterial pressure. Nephron ETA, under normal conditions, likely do not play a major role in regulation of Na excretion or systemic hemodynamics.
    Type of Medium: Online Resource
    ISSN: 1471-2369
    URL: Article
    DOI: 10.1186/1471-2369-13-166
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
    detail.hit.zdb_id: 2041348-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Insulin resistance, kidney outcomes and effects of the endothelin receptor antagonist atrasentan in patients with type 2 diabetes and chronic kidney disease
    Springer Science and Business Media LLC ; 2023
    In:  Cardiovascular Diabetology Vol. 22, No. 1 ( 2023-09-16)
    Details
    In: Cardiovascular Diabetology, Springer Science and Business Media LLC, Vol. 22, No. 1 ( 2023-09-16)
    Abstract: Insulin resistance (IR) is a pathophysiologic hallmark of type 2 diabetes and associated with the presence of chronic kidney disease (CKD). Experimental studies suggest that endothelin-1 increases IR. We assessed the association between IR and cardio-renal outcomes and the effect of the selective endothelin receptor antagonist atrasentan on IR in patients with type 2 diabetes and CKD. Methods We used data from the RADAR and SONAR trials that recruited participants with type 2 diabetes and CKD [eGFR 25–75 mL/min/1.73 m², urine albumin-to-creatinine ratio of 300–5000 mg/g]. IR was calculated using the homeostatic model assessment (HOMA-IR). The association between HOMA-IR and the pre-specified cardio-renal outcomes was assessed using multivariable Cox proportional hazards regression, and effects of atrasentan on HOMA-IR by a linear mixed effect model. Results In the SONAR trial, each log-unit increase in HOMA-IR was associated with an increased risk of the composite cardio-renal outcome [hazard ratio 1.32 (95%CI 1.09,1.60; p = 0.004)], kidney outcome [hazard ratio 1.30 (95%CI 1.00,1.68; p-value = 0.048)] , and the kidney or all-cause mortality outcome [hazard ratio 1.25 (95%CI 1.01,1.55; p-value = 0.037)]. After 12 weeks treatment in the RADAR trial (N = 123), atrasentan 0.75 mg/day and 1.25 mg/day compared to placebo reduced HOMA-IR by 19.1 (95%CI -17.4, 44.3) and 26.7% (95%CI -6.4, 49.5), respectively. In the SONAR trial (N = 1914), atrasentan 0.75 mg/day compared to placebo reduced HOMA-IR by 9.6% (95%CI 0.6, 17.9). Conclusions More severe IR is associated with increased risk of cardio-renal outcomes. The endothelin receptor antagonist atrasentan reduced IR. Trial registration RADAR trial (Reducing Residual Albuminuria in Subjects With Diabetes and Nephropathy With AtRasentan): NCT01356849. SONAR trial (The Study Of Diabetic Nephropathy With AtRasentan) NCT01858532.
    Type of Medium: Online Resource
    ISSN: 1475-2840
    URL: Article
    DOI: 10.1186/s12933-023-01964-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2093769-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Myocardial, Smooth Muscle, Nephron, and Collecting Duct Gene Targeting Reveals the Organ Sites of Endothelin A Receptor Antagonist Fluid Retention
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2013
    In:  Journal of Pharmacology and Experimental Therapeutics Vol. 346, No. 2 ( 2013-08), p. 182-189
    Details
    In: Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 346, No. 2 ( 2013-08), p. 182-189
    Type of Medium: Online Resource
    ISSN: 0022-3565 , 1521-0103
    URL: Article
    DOI: 10.1124/jpet.113.205286
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2013
    detail.hit.zdb_id: 1475023-5
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Lipopolysaccharide Upregulates Renal Shiga Toxin Receptors in a Primate Model of Hemolytic Uremic Syndrome
    S. Karger AG ; 2005
    In:  American Journal of Nephrology Vol. 25, No. 6 ( 2005), p. 536-540
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 25, No. 6 ( 2005), p. 536-540
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Although Shiga toxin (Stx) mediates classical hemolytic uremic syndrome (HUS), it is not fully understood why only some subjects exposed to Stx-expressing 〈 i 〉 Escherichia coli 〈 /i 〉 develop HUS. We have previously shown in a baboon model of Stx-mediated HUS that coadministration of lipopolysaccharide (LPS) results in an augmented host response to otherwise subtoxic Stx1 doses. We used this model to test the hypothesis that LPS upregulates renal Stx receptor (Gb 〈 sub 〉 3 〈 /sub 〉 ) expression. 〈 i 〉 Methods: 〈 /i 〉 Juvenile baboons were treated with either Stx1 (100 ng/kg), LPS (1 mg/kg as two divided doses 24 h apart), or a sham injection of saline, and sacrificed and immediately autopsied at 72 h. Renal cortical tissue Gb 〈 sub 〉 3 〈 /sub 〉 content was quantitated by lipid extraction and thin-layer chromatography, and Stx1 and Gb 〈 sub 〉 3 〈 /sub 〉 /CD77 immunostaining was assessed by quantitative immunofluorescent microscopy. 〈 i 〉 Results: 〈 /i 〉 Compared to saline-in jected controls, LPS administration resulted in a 2.2-fold increase in renal cortical Gb 〈 sub 〉 3 〈 /sub 〉 by chromatography (p 〈 0.01), a 2.5-fold increase in Stx1 staining (p = 0.003) and a 1.7-fold increase in CD77 immunostaining (p = 0.004). Stx treatment did not significantly alter either Stx or CD77 immunostaining. 〈 i 〉 Conclusion: 〈 /i 〉 These observations suggest that LPS primes the host for Stx-mediated renal injury by upregulating renal Gb 〈 sub 〉 3 〈 /sub 〉 expression.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000088523
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2005
    detail.hit.zdb_id: 1468523-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...