liu.seSearch for publications in DiVA
Change search
Refine search result
1 - 6 of 6
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Friederich-Persson, Malou
    et al.
    Uppsala University, Sweden .
    Thorn, Erik
    Gothenburg University, Sweden .
    Hansell, Peter
    Uppsala University, Sweden .
    Nangaku, Masaomi
    University of Tokyo, Japan .
    Levin, Max
    Gothenburg University, Sweden .
    Palm, Fredrik
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Health Sciences.
    Kidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress2013In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 62, no 5, p. 914-919Article in journal (Refereed)
    Abstract [en]

    Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.

  • 2.
    Karlberg, B E
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Lins, L-E
    Hermansson, K
    Efficacy and safety of telmisartan, a selective AT. Receptor antagonist, compared with enalaprilin elderly patients with primary hypertensions.1999In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 17, p. 293-302Article in journal (Refereed)
  • 3.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Connors, Stephanie G
    Mendonca, Margarida
    Welch, William J
    Wilcox, Christopher S
    Angiotensin II Type 2 Receptors and Nitric Oxide Sustain Oxygenation in the Clipped Kidney of Early Goldblatt Hypertensive Rats2008In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 51, no 2, p. 345-351Article in journal (Refereed)
    Abstract [en]

    Angiotensin-converting enzyme inhibitors (ACEIs) decrease theglomerular filtration rate and renal blood flow in the clippedkidneys of early 2-kidney, 1-clip Goldblatt hypertensive rats,but the consequences for oxygenation are unclear. We investigatedthe hypothesis that angiotensin II type 1 or angiotensin IItype 2 receptors or NO synthase mediate renal oxygenation responsesto ACEI. Three weeks after left renal artery clipping, kidneyfunction, oxygen (O2) use, renal blood flow, renal corticalblood flow, and renal cortical oxygen tension (PO2) were measuredafter acute administration of an ACEI (enalaprilat) and afteracute administration of ACEI following acute administrationof an angiotensin II type 1 or angiotensin II type 2 receptorblocker (candesartan or PD-123,319) or an NO synthase blocker(NG-nitro-L-arginine methyl ester with control of renal perfusionpressure) and compared with mechanical reduction in renal perfusionpressure to the levels after ACEI. The basal renal corticalPO2 of clipped kidneys was significantly lower than contralateralkidneys (35±1 versus 51±1 mm Hg; n=40 each). ACEIlowered renal venous PO2, cortical PO2, renal blood flow, glomerularfiltration rate, and cortical blood flow and increased the renalvascular resistance in the clipped kidney, whereas mechanicalreduction in renal perfusion pressure was ineffective. PD-123,319and NG-nitro-L-arginine methyl ester, but not candesartan, reducedthe PO2 of clipped kidneys and blocked the fall in PO2 withacute ACEI administration. In conclusion, oxygen availabilityin the clipped kidney is maintained by angiotensin II generation,angiotensin II type 2 receptors, and NO synthase. This disclosesa novel mechanism whereby angiotensin can prevent hypoxia ina kidney challenged with a reduced perfusion pressure.

  • 4.
    Palm, Fredrik
    et al.
    Uppsala universitet, Integrativ Fysiologi.
    Onozato, Maristela
    Georgetown University.
    Welch, William J
    Georgetown University.
    Wilcox, Christopher S
    Georgetown University.
    Blood pressure, blood flow, and oxygenation in the clipped kidney of chronic 2-kidney, 1-clip rats: effects of tempol and Angiotensin blockade2010In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 55, no 2, p. 298-304Article in journal (Refereed)
    Abstract [en]

    Angiotensin II maintains renal cortical blood flow and renal oxygenation in the clipped kidney of early 2-kidney, 1-clip Goldblatt hypertensive (2K,1C) rats. The involvement of Ang II is believed to decline, whereas oxidative stress increases during the progression of 2K,1C hypertension. We investigated the hypothesis that the acute administration of drugs to inhibit reactive oxygen species (Tempol), angiotensin II type 1 receptors (candesartan), or angiotensin-converting enzyme (enalaprilat) lowers mean arterial pressure and increases kidney blood flow and oxygenation in the clipped kidney of chronic 2K,1C rats in contrast to sham controls. Twelve months after left renal artery clipping or sham, mean arterial pressure, renal cortical blood flow, and renal cortical and medullary oxygen tension were measured after acute administration of Tempol followed by enalaprilat or candesartan followed by enalaprilat. The mean arterial pressure of the 2K,1C rat was reduced by candesartan (-9%) and, more effectively, by Tempol (-35%). All of the applied treatments had similar blood pressure-lowering effects in sham rats (average: -21%). Only Tempol increased cortical blood flow (+35%) and cortical and medullary oxygen tensions (+17% and +94%, respectively) in clipped kidneys of 2K,1C rats. Administration of enalaprilat had no additional effect, except for a modest reduction in cortical blood flow in the clipped kidney of 2K,1C rats when coadministered with candesartan (-10%). In conclusion, acute administration of Tempol is more effective than candesartan in reducing the mean arterial blood pressure and improving renal blood perfusion and oxygenation in the clipped kidney of chronic 2K,1C rats.

  • 5.
    Persson, Patrik
    et al.
    Uppsala University, Sweden .
    Fasching, Angelica
    Uppsala University, Sweden .
    Teerlink, Tom
    Vrije University of Amsterdam, Netherlands .
    Hansell, Peter
    Uppsala University, Sweden .
    Palm, Fredrik
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Health Sciences.
    L-Citrulline, But Not L-Arginine, Prevents Diabetes Mellitus-Induced Glomerular Hyperfiltration and Proteinuria in Rat2014In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 64, no 2, p. 323-329Article in journal (Refereed)
    Abstract [en]

    Diabetes mellitus-induced oxidative stress causes increased renal oxygen consumption and intrarenal tissue hypoxia. Nitric oxide is an important determinant of renal oxygen consumption and electrolyte transport efficiency. The present study investigates whether L-arginine or L-citrulline to promote nitric oxide production prevents the diabetes mellitus-induced kidney dysfunction. Glomerular filtration rate, renal blood flow, in vivo oxygen consumption, tissue oxygen tension, and proteinuria were investigated in control and streptozotocin-diabetic rats with and without chronic L-arginine or L-citrulline treatment for 3 weeks. Untreated and L-arginine-treated diabetic rats displayed increased glomerular filtration rate (2600 +/- 162 versus 1599 +/- 127 and 2290 +/- 171 versus 1739 +/- 138 mu L/min per kidney), whereas L-citrulline prevented the increase (1227 +/- 126 versus 1375 +/- 88 mu L/min per kidney). Filtration fraction was increased in untreated diabetic rats because of the increase in glomerular filtration rate but not in L-arginine-or L-citrulline-treated diabetic rats. Urinary protein excretion was increased in untreated and L-arginine-treated diabetic rats (142 +/- 25 versus 75 +/- 7 and 128 +/- 7 versus 89 +/- 7 mu g/min per kidney) but not in diabetic rats administered L-citrulline (67 +/- 7 versus 61 +/- 5 mu g/min per kidney). The diabetes mellitus-induced tissue hypoxia, because of elevated oxygen consumption, was unaltered by any of the treatments. L-citrulline administered to diabetic rats increases plasma l-arginine concentration, which prevents the diabetes mellitus-induced glomerular hyperfiltration, filtration fraction, and proteinuria, possibly by a vascular effect.

  • 6.
    Rahman, M
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Östergötlands Läns Landsting, Pain and Occupational Centre, Occupational and Environmental Medicine Centre.
    Tondel, Martin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Östergötlands Läns Landsting, Pain and Occupational Centre, Occupational and Environmental Medicine Centre.
    Ahmad, A
    Chowdhury, IA
    Faruquee, M
    Axelson, Olav
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Östergötlands Läns Landsting, Pain and Occupational Centre, Occupational and Environmental Medicine Centre.
    Hypertension and arsenic exposure in Bangladesh.  1999In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 33, p. 74-78Article in journal (Refereed)
1 - 6 of 6
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf