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
    Regulation of Renin Secretion and Expression in Mice Deficient in β1- and β2-Adrenergic Receptors
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Hypertension Vol. 50, No. 1 ( 2007-07), p. 103-109
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 50, No. 1 ( 2007-07), p. 103-109
    Abstract: The present experiments were performed in β1/β2-adrenergic receptor–deficient mice (β1/β2ADR −/− ) to assess the role of β-adrenergic receptors in basal and regulated renin expression and release. On a control diet, plasma renin concentration (in ng angiotensin I per mL per hour), determined in tail vein blood, was significantly lower in β1/β2ADR −/− than in wild-type (WT) mice (222±65 versus 1456±335; P 〈 0.01). Renin content and mRNA were 77% and 65±5% of WT. Plasma aldosterone (in picograms per mL) was also significantly reduced (420±36 in β1/β2ADR −/− versus 692±59 in WT). A low-salt diet (0.03%) for 1 week increased plasma renin concentration significantly in both β1/β2ADR −/− and WT mice (to 733±54 and 2789±555), whereas a high-salt diet (8%) suppressed it in both genotypes (to 85±24 in β1/β2ADR −/− and to 676±213 in WT). The absolute magnitude of salt-induced changes of plasma renin concentration was markedly greater in WT mice. Acute stimulation of renin release by furosemide, quinaprilat, captopril, or candesartan caused significant increases of plasma renin concentration in both β1/β2ADR −/− and WT mice, but again the absolute changes were greater in WT mice. We conclude that maintenance of normal levels of renin synthesis and release requires tonic β-adrenergic receptor activation. In the chronic absence of β-adrenergic receptor input, the size of the releasable renin pool decreases with a concomitant reduction in the magnitude of the plasma renin concentration changes caused by variations of salt intake or acute stimulation with furosemide, angiotensin-converting enzyme, or angiotensin type 1 receptor inhibition, but regulatory responsiveness is nonetheless maintained.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.087577
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 2094210-2
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 2
    Online Resource
    Online Resource
    Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Renal Physiology Vol. 288, No. 6 ( 2005-06), p. F1125-F1132
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 288, No. 6 ( 2005-06), p. F1125-F1132
    Abstract: The present study was undertaken to determine whether the severity of renal failure or hypertension in homozygous cyclooxygenase (COX)-2-deficient (COX-2−/−) mice affected by genetic background or gender. COX-2 deletion was introduced into three congenic genetic backgrounds, 129/Sv (129/COX-2−/−), C57/BL6 (C57/COX-2−/−), and BALB/c (BALB/COX-2−/−), by backcrossing the original mixed-background knockout mice with the respective inbred strains for 9 or 10 generations. Evaluation of the severity of hypertension and renal failure was performed in knockout and wild-type mice at the age of 2.5–3.5 mo. Blood pressure measured by tail-cuff plethysmography was significantly elevated in the male 129/COX-2−/− mice (165.8 ± 9.2 vs. 116 ± 5.1 mmHg, P 〈 0.05), and to a much lesser extent in the female 129/COX-2−/− mice (127.4 ± 3.3 vs. 102.4 ± 3.3), whereas it was unchanged in the C57- or BALB/COX-2−/− mice regardless of gender. Urinary excretion of albumin, determined by EIA, was remarkably increased in the 129/COX-2−/− (16.4 ± 4.1 vs. 0.16 ± 0.043 mg albumin/mg creatinine, P 〈 0.001), and to a lesser extent in the male C57/COX-2−/− mice (0.595 ± 0.416 vs. 0.068 ± 0.019). Albumin excretion was not elevated in the male BALB/COX-2−/− or in female COX-2−/− mice on any of the three genetic backgrounds. Histological analysis showed abundant protein casts, dilated tubules, and infiltration of inflammatory cells in the male 129/COX-2−/− mice, but not in COX-2−/− mice in other strains or gender. However, the presence of small glomeruli in the nephrogenic zone was observed in all strains of COX-2 knockout mice, regardless of genetic background and gender. Therefore, we conclude that the severity of hypertension and renal failure in COX-2-deficient mice is influenced by genetic background and gender, whereas the incomplete maturation of outer cortical nephrons appears to be independent of genetic background effects.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00219.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477287-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 3
    Online Resource
    Online Resource
    Inhibition of macula densa-stimulated renin secretion by pharmacological blockade of cyclooxygenase-2
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Renal Physiology Vol. 277, No. 5 ( 1999-11-01), p. F706-F710
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 277, No. 5 ( 1999-11-01), p. F706-F710
    Abstract: Previous results from our laboratory have shown that in the isolated perfused juxtaglomerular apparatus, nonselective inhibitors of cyclooxygenase (COX) activity prevent the stimulation of renin secretion by a reduction in luminal NaCl concentration at the macula densa. The present studies were performed to examine which COX isoform is involved in NaCl-dependent renin secretion. In the absence of COX inhibitors, a reduction in luminal NaCl (from Na 141/Cl 120 mM to Na 26/Cl 7 mM) caused an increase in renin secretion rate from 4.5 ± 1.8 to 26.1 ± 7.4 nGU/min ( P 〈 0.01, n = 19). The presence of the COX-1 inhibitor valerylsalicylate (500 μM) in lumen and bath did not affect the stimulation of renin secretion by a reduction in luminal NaCl concentration (5 ± 1.8 nGU/min at high NaCl, and 30.5 ± 9.4 nGU/min at low NaCl; P 〈 0.01, n = 8). In contrast, the specific COX-2 inhibitor NS-398 (50 μM) in lumen and bath abolished the stimulating effect of low luminal NaCl (12.8 ± 3.9 nGU/min at high NaCl, and 10.7 ± 3.1 nGU/min at low NaCl; NS, n = 15). The finding that COX-2 is critically involved in macula densa control of renin secretion indicates that the COX-2-expressing epithelial cells in the tubuloglomerular contact area are a likely source of prostaglandins participating in the signaling pathway between the macula densa and renin-producing granular cells.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1999.277.5.F706
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477287-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 4
    Online Resource
    Online Resource
    Differential regulation of COX-2 expression in the kidney by lipopolysaccharide: role of CD14
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Renal Physiology Vol. 277, No. 1 ( 1999-07-01), p. F10-F16
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 277, No. 1 ( 1999-07-01), p. F10-F16
    Abstract: Induction of the inducible cyclooxygenase isoform COX-2 is likely to be an important mechanism for increased prostaglandin production in renal inflammation. We examined the effect of lipopolysaccharide (LPS) on regional renal COX-2 expression in the rat. In the inner medulla, LPS injection (4 mg/kg ip) induced a twofold and 2.5-fold increase in the levels of COX-2 mRNA and COX-2 protein, respectively. In contrast, COX-2 expression in the renal cortex was not significantly altered. COX-2 promoter transgenic mice were created using the 2.7-kb flanking region of the rat COX-2 gene. In these animals, LPS injection induced reporter gene expression predominately in the inner medulla. The LPS receptor CD14, usually regarded as a monocyte/macrophage-specific marker, was found to be abundantly expressed in the inner medulla and in dissected inner medullary collecting duct (IMCD) cells, suggesting that it may mediate medullary COX-2 induction. CD14 was present only at low levels in cortex and cortical segments, including glomeruli. In cultured cells, it was abundant in mouse IMCD (mIMCD-K2) cells and renal medullary interstitial cells, but largely undetectable in mesangial cells and M1 cells, a cell line derived from mouse cortical collecting ducts. In the mIMCD-K2 cell line, LPS significantly induced COX-2 mRNA expression, with concomitant induction of CD14. LPS-stimulated COX-2 expression was reduced by the addition of an anti-CD14 monoclonal antibody to the culture medium. These results demonstrate that LPS selectively stimulates COX-2 expression in the renal inner medulla through a CD14-dependent mechanism.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1999.277.1.F10
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477287-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 5
    Online Resource
    Online Resource
    MAPK Mediation of Hypertonicity-stimulated Cyclooxygenase-2 Expression in Renal Medullary Collecting Duct Cells
    Elsevier BV ; 2000
    In:  Journal of Biological Chemistry Vol. 275, No. 30 ( 2000-07), p. 23281-23286
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 275, No. 30 ( 2000-07), p. 23281-23286
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M910237199
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2000
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 6
    Online Resource
    Online Resource
    Hypertonic Induction of COX-2 in Collecting Duct Cells by Reactive Oxygen Species of Mitochondrial Origin
    Elsevier BV ; 2005
    In:  Journal of Biological Chemistry Vol. 280, No. 41 ( 2005-10), p. 34966-34973
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 280, No. 41 ( 2005-10), p. 34966-34973
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M502430200
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2005
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 7
    Online Resource
    Online Resource
    Macula Densa Control of Renin Secretion and Glomerular Vascular Tone: Evidence for Common Cellular Mechanisms
    S. Karger AG ; 1986
    In:  Kidney and Blood Pressure Research Vol. 9, No. 4 ( 1986), p. 193-203
    Details
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 9, No. 4 ( 1986), p. 193-203
    Abstract: The macula densa is believed to function as a sensor for control of intrarenal vascular tone and renin secretion. Increases in flow rate through the loop of Henle or increases in distal tubular fluid NaCl concentration result in an increase in local vascular tone and a decrease in glomerular filtration rate, the tubuloglomerular feedback (TGF) mechanism. Increases in distal NaCl concentration are also believed to inhibit renin secretion. Evidence will be reviewed that suggests that these two processes may be activated concurrently and may share common cellular mechanisms. Similarities in the sensor step include a similar pattern of ion specificity, with both responses being relatively anion specific but showing little cation specificity. TGF responses are inhibitable by furosemide, and the renin secretion produced by furosemide seems to be in part macula densa dependent. There appear also to be common features in the effector step of both responses. Increases in intracellular calcium are implicated in both the vasoconstrictive response seen with increased macula densa NaCl concentration and in inhibition of renin secretion. Changes in cyclic AMP may play a role in the converse responses.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    URL: Article
    DOI: 10.1159/000173084
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1986
    detail.hit.zdb_id: 1482922-8
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 8
    Online Resource
    Online Resource
    Salt sensitivity of blood pressure in NKCC1-deficient mice
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Renal Physiology Vol. 295, No. 4 ( 2008-10), p. F1230-F1238
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 295, No. 4 ( 2008-10), p. F1230-F1238
    Abstract: NKCC1 is a widely expressed isoform of the Na-2Cl-K cotransporter that mediates several direct and indirect vascular effects and regulates expression and release of renin. In this study, we used NKCC1-deficient (NKCC1 −/− ) and wild-type (WT) mice to assess day/night differences of blood pressure (BP), locomotor activity, and renin release and to study the effects of high (8%) or low (0.03%) dietary NaCl intake on BP, activity, and the renin/aldosterone system. On a standard diet, 24-h mean arterial blood pressure (MAP) and heart rate determined by radiotelemetry, and their day/night differences, were not different in NKCC1 −/− and WT mice. Spontaneous and wheel-running activities in the active night phase were lower in NKCC1 −/− than WT mice. In NKCC1 −/− mice on a high-NaCl diet, MAP increased by 10 mmHg in the night without changes in heart rate. In contrast, there was no salt-dependent blood pressure change in WT mice. MAP reductions by hydralazine (1 mg/kg) or isoproterenol (10 μg/mouse) were significantly greater in NKCC1 −/− than WT mice. Plasma renin (PRC; ng ANG I·ml −1 ·h −1 ) and aldosterone (aldo; pg/ml) concentrations were higher in NKCC1 −/− than WT mice (PRC: 3,745 ± 377 vs. 1,245 ± 364; aldo: 763 ± 136 vs. 327 ± 98). Hyperreninism and hyperaldosteronism were found in NKCC1 −/− mice during both day and night. High Na suppressed PRC and aldosterone in both NKCC1 −/− and WT mice, whereas a low-Na diet increased PRC and aldosterone in WT but not NKCC1 −/− mice. We conclude that 24-h MAP and MAP circadian rhythms do not differ between NKCC1 −/− and WT mice on a standard diet, probably reflecting a balance between anti- and prohypertensive factors, but that blood pressure of NKCC1 −/− mice is more sensitive to increases and decreases of Na intake.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.90392.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477287-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 9
    Online Resource
    Online Resource
    Cyclooxygenase-2 is expressed in bladder during fetal development and stimulated by outlet obstruction
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Renal Physiology Vol. 273, No. 4 ( 1997-10-01), p. F538-F544
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 273, No. 4 ( 1997-10-01), p. F538-F544
    Abstract: Studies were undertaken to assess expression of inducible cyclooxygenase (COX)-2 in bladder during fetal development and COX-1 and COX-2 expression after outlet obstruction. Bladder tissue or bladder progenitor tissue was harvested from CD-1 murine embryos at embryonic days 11.5( E11.5), E14.5, E17.5, E20.5 (newborn), and from adult. Bladder obstruction was created in adult female mice by ligating the urethra, and bladders were harvested after 3–24 h of obstruction. Gene expression was assessed by semiquantitative reverse transcription-polymerase chain reaction and Western blotting. COX-2 was highly expressed at the early stages of bladder development and declined progressively throughout gestation. In adult bladder, both COX-1 and COX-2 were detectable at low levels under basal conditions. An ∼30-fold increase in COX-2 mRNA was seen after 24 h of obstruction. In contrast, COX-1 did not change with obstruction. COX-2 mRNA levels peaked at 6 h of obstruction. In regional bladder-distention models, COX-2 induction was confined to the area of distention. Bladder outlet obstruction stimulates COX-2 expression dramatically, reactivating a gene that is highly expressed during fetal development.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1997.273.4.F538
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477287-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 10
    Online Resource
    Online Resource
    Tubular control of renin synthesis and secretion
    Springer Science and Business Media LLC ; 2013
    In:  Pflügers Archiv - European Journal of Physiology Vol. 465, No. 1 ( 2013-1), p. 39-51
    Details
    In: Pflügers Archiv - European Journal of Physiology, Springer Science and Business Media LLC, Vol. 465, No. 1 ( 2013-1), p. 39-51
    Type of Medium: Online Resource
    ISSN: 0031-6768 , 1432-2013
    URL: Article
    DOI: 10.1007/s00424-012-1115-x
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 1463014-X
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
Nothing or not found what you are looking for? Please check your search query or use the Interlibrary Loan Search.
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages