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
Filter
Material
Publisher
Person/Organisation
Language
Years
FID
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Renal endosomes contain angiotensin peptides, converting enzyme, and AT 1A receptors
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Renal Physiology Vol. 277, No. 2 ( 1999-08-01), p. F303-F311
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 277, No. 2 ( 1999-08-01), p. F303-F311
    Abstract: Kidney cortex and proximal tubular angiotensin II (ANG II) levels are greater than can be explained on the basis of circulating ANG II, suggesting intrarenal compartmentalization of these peptides. One possible site of intracellular accumulation is the endosomes. In the present study, we tested for endosomal ANG I, ANG II, angiotensin type 1A receptor (AT 1A ), and angiotensin converting enzyme (ACE) activity and determined whether these levels are regulated by salt intake. Male Sprague-Dawley rats were fed chow containing either high or low dietary sodium for 10–14 days. Blood and kidneys were harvested and processed for measurement of plasma, kidney, and renal intermicrovillar cleft and endosomal angiotensin levels. Kidney ANG I averaged 179 ± 20 fmol/g and ANG II averaged 258 ± 36 fmol/g in rats fed a high-sodium diet and were significantly higher, averaging 347 ± 58 fmol/g and 386 ± 55 fmol/g, respectively, in rats fed a low-salt diet. Renal intermicrovillar clefts and endosomes contained ANG I and ANG II. Intermicrovillar cleft ANG I and ANG II levels averaged 8.4 ± 2.6 and 74 ± 26 fmol/mg, respectively, in rats fed a high-salt diet and 7.6 ± 1.7 and 70 ± 25 fmol/mg in rats fed a low-salt diet. Endosomal ANG I and ANG II levels averaged 12.3 ± 4.4 and 43 ± 19 fmol/mg, respectively, in rats fed a high-salt diet, and these levels were similar to those observed in rats fed a low-salt diet. Renal endosomes from rats fed a low-salt diet demonstrated significantly more AT 1A receptor binding compared with rats fed a high-salt diet. ACE activity was detectable in renal intermicrovillar clefts and was 2.5-fold higher than the levels observed in renal endosomes. Acute enalaprilat treatment decreased ACE activity in renal intermicrovillar clefts by 90% and in renal endosomes by 84%. Likewise, intermicrovillar cleft and endosomal ANG II levels decreased by 61% and 52%, respectively, in enalaprilat-treated animals. These data demonstrate the presence of intact angiotensin peptides and ACE activity in renal intermicrovillar clefts and endosomes, indicating that intact angiotensin peptides are formed and/or trafficked through intracellular endosomal compartments and are dependent on ACE activity.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1999.277.2.F303
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477287-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Thomas George Coleman, PhD (1940–2021)
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Hypertension Vol. 77, No. 6 ( 2021-06), p. 1800-1803
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 77, No. 6 ( 2021-06), p. 1800-1803
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.121.17287
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Abstract P031: Reduced Augmentation Of The Intrarenal Renin-angiotensin System (ras), Lower Systolic Blood Pressure, And Preserved Renal Function In Female Compared To Male Rats With Unilateral Renal Artery Stenosis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Hypertension Vol. 76, No. Suppl_1 ( 2020-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. Suppl_1 ( 2020-09)
    Abstract: Despite growing evidence of sex differences in the progression of hypertension, there are no guidelines that differentiate treatment between men and women. Intrarenal renin-angiotensin system (RAS) activation and tissue injury in 2-kidney, 1-clip (2K1C) hypertensive rats have been characterized in previous studies of male but not female rats. To evaluate possible sex differences in response to renovascular hypertension, urinary angiotensinogen (uAGT) excretion, systolic blood pressure (BP), urinary protein excretion, and renal function were assessed in female rats.Female (n=8) and male (n=6) rats underwent placement of a 0.2 mm clip on the left renal artery to simulate unilateral renal artery stenosis. BP was measured by tail-cuff plethysmography, and clearance studies were conducted in anesthetized rats to assess renal function. Urine protein concentration was determined by pyrogallol red method. uAGT was measured by ELISA as an index of intrarenal RAS activity. Systolic BP increased from 120±1 to 176±8 mmHg, and urinary protein excretion reached 20.2±5.6 mg/day in female rats. Although uAGT excretion increased from 13.2±7.7 ng/day to 74.1±29.9 ng/day in female rats, male rats had a significantly higher uAGT excretion of 1572.6±750 ng/day. Nonclipped kidneys exhibited more uAGT excretion compared to clipped kidneys, consistent with previous findings in males. Although 2K1C female rats demonstrate significantly lower renal function than sham females, they show more preserved renal function than male rats. Female rats also demonstrate significantly lower increases in systolic BP and urinary protein excretion compared to male rats. The data support substantial sex-dependent differences in renal responses to unilateral renal artery stenosis. The results show substantial increases in systolic BP, uAGT, and urinary protein excretion and decreased renal function after renal artery clipping in females, but the magnitude of the changes is markedly lower than in males. Nonclipped kidneys of both sexes exhibit greater uAGT excretion than clipped kidneys. Notably, females show less augmentation of the intrarenal RAS compared to male rats in renovascular hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.76.suppl_1.P031
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Abstract 051: The Role of Immunological Memory in Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 66, No. suppl_1 ( 2015-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. suppl_1 ( 2015-09)
    Abstract: Immunological memory provides protection to repeated antigen challenges and is a cardinal feature of adaptive immunity. We have previously shown that adaptive immunity contributes to hypertension and have observed memory T cells in several models. We hypothesized that memory T cells contribute to long-term renal damage in response to repeated hypertensive challenges. To impose repeated episodes of hypertension, we treated C57BL/6 mice with L-NAME (0.5mg/ml) in drinking water for two weeks, allowed a two-week normotensive interval and then fed high salt (4% NaCl) for three weeks. L-NAME followed by high salt increased SBP to 151 ± 14 mmHg and caused a two-fold increase in CD4 + and CD8 + memory T cells in the kidney and bone marrow, as identified by the surface marker CD44hi. Intracellular staining showed that memory T cells were predominant sources of the inflammatory cytokines IL-17A and IFN-γ. Development and reactivation of memory T cells require the interaction of CD27 on T cells with CD70 on antigen presenting cells. Flow cytometry revealed that L-NAME/High salt increased expression of CD70 on splenic macrophages by 5-fold and dendritic cells by 3-fold. Because memory T cells are a major source of IFN-γ, we examined the hypertensive response to the L-NAME/high salt protocol in IFN-γ -/- mice. The hypertension caused by L-NAME was identical between WT, CD70 -/- and IFN-γ -/- mice. In contrast, the hypertension induced by subsequent salt administration was markedly attenuated in CD70 -/- mice (123 ± 1.3 mmHg, p 〈 0.02). Likewise, mice lacking IFN-γ developed blunted hypertension during the salt-feeding phase (127.6 ± 5.5 mmHg, p 〈 0.04). Interestingly, CD70 -/- and IFN-γ -/- mice failed to develop memory T cell formation in the kidney. The L-NAME/high salt caused striking albuminuria and increased urinary N-gal in WT mice, and these were absent in CD70 -/- and IFN-γ -/- mice. In contrast, L-NAME/high salt had no effect on renal angiotensinogen levels. Thus, repeated hypertensive stimuli lead to accumulation of long-lived effector memory T cells that are major sources of inflammatory cytokines, which in turn promote renal dysfunction, salt sensitivity and hypertension. These studies provide further insight into how the adaptive immune system promotes hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.66.suppl_1.051
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Urine Angiotensinogen and Salt- and Potassium-Sensitivity of Blood Pressure
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Journal of Hypertension Vol. 33, No. Supplement 2 ( 2015-06), p. e4-
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. Supplement 2 ( 2015-06), p. e4-
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/01.hjh.0000469731.90492.8a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2017684-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Ang II Accumulation in Rat Renal Endosomes During Ang II-Induced Hypertension : Role of AT 1 Receptor
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Hypertension Vol. 39, No. 1 ( 2002-01), p. 116-121
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 1 ( 2002-01), p. 116-121
    Abstract: Hypertension induced by long-term infusion of angiotensin II (Ang II) is associated with augmented intrarenal Ang II levels to a greater extent than can be explained on the basis of the circulating Ang II levels. Although part of this augmentation is due to AT 1 receptor–dependent internalization, the intracellular compartments involved in this Ang II accumulation remain unknown. In the present study, we sought to determine whether Ang II trafficking into renal cortical endosomes is increased during Ang II hypertension, and if so, whether the AT 1 receptor antagonist, candesartan, prevents this accumulation. Compared with controls (n=12; 114±2 mm Hg), Ang II-infused rats (n=12; 80 ng/kg/min, SC, for 13 days) developed hypertension with systolic blood pressure rising to 185±4 mm Hg by Day 12. In Ang II hypertensive rats, plasma renin activity was suppressed, whereas plasma and kidney Ang II levels were increased by 3-fold (348±58 versus 119±16 fmol/mL) and 2-fold (399±39 versus 186±26 fmol/g). Intracellular endosomal Ang II levels were increased by more than 10-fold (1100±283 versus 71±12 fmol/mg protein), whereas intermicrovillar cleft Ang II levels were increased by more than 2-fold (88±22 versus 37±7 fmol/mg protein). Flow cytometric analysis detected significant increases in AT 1A receptor antibody binding in endosomal and intermicrovillar clefts of Ang II–infused rats. The hypertension induced by Ang II was prevented in rats treated concurrently with candesartan (2 mg/kg/d, 119±3 mm Hg). Candesartan treatment (n=8) also prevented increases in kidney (215±19 fmol/g), endosomal (96±29 fmol/mg protein), and intermicrovillar cleft Ang II levels (11±2 fmol/mg protein). These results indicate that there is substantial intracellular accumulation of angiotensin peptides in renal cortical endosomes during Ang II–dependent hypertension via an AT 1 receptor–mediated process.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hy0102.100780
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Evaluation of the single nephron glomerular filtration coefficient in the dog
    Elsevier BV ; 1977
    In:  Kidney International Vol. 12, No. 2 ( 1977-08), p. 137-149
    Details
    In: Kidney International, Elsevier BV, Vol. 12, No. 2 ( 1977-08), p. 137-149
    Type of Medium: Online Resource
    ISSN: 0085-2538
    URL: Article
    DOI: 10.1038/ki.1977.91
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1977
    detail.hit.zdb_id: 2007940-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    The role of IL-6 in the physiologic versus hypertensive blood pressure actions of angiotensin II
    Wiley ; 2015
    In:  Physiological Reports Vol. 3, No. 10 ( 2015-10), p. e12595-
    Details
    In: Physiological Reports, Wiley, Vol. 3, No. 10 ( 2015-10), p. e12595-
    Type of Medium: Online Resource
    ISSN: 2051-817X
    URL: Article
    DOI: 10.14814/phy2.12595
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2724325-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Intracellular ANG II induces cytosolic Ca 2+ mobilization by stimulating intracellular AT 1 receptors in proximal tubule cells
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Renal Physiology Vol. 290, No. 6 ( 2006-06), p. F1382-F1390
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 290, No. 6 ( 2006-06), p. F1382-F1390
    Abstract: Intracellular ANG II induces biological effects in nonrenal cells, but it is not known whether it plays a physiological role in renal proximal tubule cells (PTCs). PTCs express angiotensinogen, renin, and angiotensin-converting enzyme mRNAs, suggesting the presence of high levels of intracellular ANG II. We determined if microinjection of ANG II directly in single PTCs increases intracellular calcium concentration ([Ca 2+ ] i ) and, if so, elucidated the cellular mechanisms involved. Changes in [Ca 2+ ] i responses were studied by fluorescence imaging using the Ca 2+ indicator fluo 3. ANG II (1 nM) was microinjected directly in the cells, whereas cell-surface angiotensin type 1 (AT 1 ) receptors were blocked by losartan (10 μM). When ANG II (1 nM) was added to the perfusate, there was a marked increase in [Ca 2+ ] i that was blocked by extracellular losartan. With losartan in the perfusate, intracellular microinjection of ANG II elicited a robust increase in cytoplasmic [Ca 2+ ] i that peaked at 30 s (basal: 2.2 ± 0.3 vs. ANG II: 14.9 ± 0.4 relative fluorescence units; P 〈 0.01). Chelation of extracellular Ca 2+ with EGTA (2 mM) did not alter microinjected ANG II-induced [Ca 2+ ] i responses (Ca 2+ free + ANG II: 12.3 ± 2.6 relative fluorescence units, not significant vs. ANG II); however, pretreatment with thapsigargin to deplete intracellular Ca 2+ stores or with U-73122 to inhibit phospholipase C (1 μM each) markedly attenuated microinjected ANG II-induced [Ca 2+ ] i responses. Combined microinjection of ANG II and losartan abolished [Ca 2+ ] i responses, whereas a combination of ANG II and PD-123319 had no effect. These data demonstrate for the first time that direct microinjection of ANG II in single PTCs increases [Ca 2+ ] i by stimulating intracellular AT 1 receptors and releases Ca 2+ from intracellular stores, suggesting that intracellular ANG II may play a physiological role in PTC function.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00269.2005
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477287-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Contribution of renal purinergic receptors to renal vasoconstriction in angiotensin II-induced hypertensive rats
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Renal Physiology Vol. 300, No. 6 ( 2011-06), p. F1301-F1309
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 300, No. 6 ( 2011-06), p. F1301-F1309
    Abstract: To investigate the participation of purinergic P2 receptors in the regulation of renal function in ANG II-dependent hypertension, renal and glomerular hemodynamics were evaluated in chronic ANG II-infused (14 days) and Sham rats during acute blockade of P2 receptors with PPADS. In addition, P2X1 and P2Y1 protein and mRNA expression were compared in ANG II-infused and Sham rats. Chronic ANG II-infused rats exhibited increased afferent and efferent arteriolar resistances and reductions in glomerular blood flow, glomerular filtration rate (GFR), single-nephron GFR (SNGFR), and glomerular ultrafiltration coefficient. PPADS restored afferent and efferent resistances as well as glomerular blood flow and SNGFR, but did not ameliorate the elevated arterial blood pressure. In Sham rats, PPADS increased afferent and efferent arteriolar resistances and reduced GFR and SNGFR. Since purinergic blockade may influence nitric oxide (NO) release, we evaluated the role of NO in the response to PPADS. Acute blockade with N ω -nitro-l-arginine methyl ester (l-NAME) reversed the vasodilatory effects of PPADS and reduced urinary nitrate excretion (NO 2 − /NO 3 − ) in ANG II-infused rats, indicating a NO-mediated vasodilation during PPADS treatment. In Sham rats, PPADS induced renal vasoconstriction which was not modified by l-NAME, suggesting blockade of a P2X receptor subtype linked to the NO pathway; the response was similar to that obtained with l-NAME alone. P2X1 receptor expression in the renal cortex was increased by chronic ANG II infusion, but there were no changes in P2Y1 receptor abundance. These findings indicate that there is an enhanced P2 receptor-mediated vasoconstriction of afferent and efferent arterioles in chronic ANG II-infused rats, which contributes to the increased renal vascular resistance observed in ANG II-dependent hypertension.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00367.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477287-5
    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...