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  • 1.
    Liss, Per
    et al.
    Uppsala universitet, Institutionen för onkologi, radiologi och klinisk immunologi.
    Aukland, Knut
    Carlsson, Per-Ola
    Institutionen för medicinsk cellbiologi.
    Palm, Fredrik
    Institutionen för medicinsk cellbiologi.
    Hansell, Peter
    Institutionen för medicinsk cellbiologi.
    Influence of iothalamate on renal medullary perfusion and oxygenation in the rat.2005In: Acta Radiologica, ISSN 0284-1851, E-ISSN 1600-0455, Vol. 46, no 8, p. 823-9Article in journal (Other academic)
  • 2.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Bergqvist, David
    Institutionen för kirurgiska vetenskaper.
    Carlsson, Per-Ola
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Hellberg, Olof
    Institutionen för medicinska vetenskaper.
    Nyman, Rickard
    Institutionen för onkologi, radiologi och klinisk immunologi.
    Hansell, Peter
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Liss, Per
    Institutionen för onkologi, radiologi och klinisk immunologi.
    The effects of carbon dioxide versus ioxaglate in the rat kidney.2005In: Journal of Vascular and Interventional Radiology, ISSN 1051-0443, E-ISSN 1535-7732, Vol. 16, no 2 Pt 1, p. 269-74Article in journal (Refereed)
  • 3.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Buerk, Donald G.
    Carlsson, Per-Ola
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Hansell, Peter
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Liss, Per
    Uppsala universitet, Institutionen för onkologi, radiologi och klinisk immunologi.
    Reduced nitric oxide concentration in the renal cortex of streptozotocin-induced diabetic rats: effects on renal oxygenation and microcirculation2005In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 54, no 11, p. 3282-7Article in journal (Refereed)
    Abstract [en]

    Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.

  • 4.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Carlsson, Per-Ola
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Thick ascending tubular cells in the loop of Henle: regulation of electrolyte homeostasis.2005In: International Journal of Biochemistry and Cell Biology, ISSN 1357-2725, E-ISSN 1878-5875, Vol. 37, no 8, p. 1554-9Article in journal (Refereed)
  • 5.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Carlsson, Per-Ola
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Fasching, Angelica
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Hansell, Peter
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Liss, Per
    Uppsala universitet, Enheten för radiologi.
    Diabetes-induced decrease in renal oxygen tension: effects of an altered metabolism2006In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 578, p. 161-166Article in journal (Refereed)
    Abstract [en]

    During conditions with experimental diabetes mellitus, it is evident that several alterations in renal oxygen metabolism occur, including increased mitochondrial respiration and increased lactate accumulation in the renal tissue. Consequently, these alterations will contribute to decrease the interstitial pO2, preferentially in the renal medulla of animals with sustained long-term hyperglycemia.

  • 6.
    Sällström, Johan
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Carlsson, Per-Ola
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Fredholm, Bertil B
    Larsson, Erik
    Uppsala universitet, Institutionen för genetik och patologi.
    Persson, Erik
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Palm, Fredrik
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Diabetes-induced hyperfiltration in adenosine A(1)-receptor deficient mice lacking the tubuloglomerular feedback mechanism2007In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 190, no 3, p. 253-259Article in journal (Refereed)
    Abstract [en]

    Aims: Glomerular hyperfiltration is commonly found in diabetic patients early after the onset of disease. This is one of the first indications of the development of progressive diabetic nephropathy. It has been proposed that glomerular hyperfiltration is caused by decreased delivery of electrolytes to the macula densa due to the increased sodium and glucose reabsorption in the proximal tubule, which would increase the glomerular filtration rate (GFR) via the tubuloglomerular feedback (TGF) mechanism. In this study, we investigated the role of TGF in diabetes-induced glomerular hyperfiltration by inducing diabetes in adenosine A1-receptor knockout (A1AR−/−) mice known to lack a functional TGF mechanism.

    Methods: Diabetes was induced by alloxan (75 mg kg−1 bw) injected into the tail vein. The 24-hour urinary electrolyte excretion was measured in metabolic cages, the GFR determined by inulin clearance under isoflurane-anaesthesia, and histological changes evaluated.

    Results: All alloxan-treated animals developed hyperglycaemia (≥20 mm). Normoglycaemic animals had a similar GFR independent of genotype (A1AR+/+ 9.3 ± 0.5 vs. A1AR−/− 10.1 ± 0.8 μL min−1g−1 bw) and diabetes resulted in similar glomerular hyperfiltration in both groups (A1AR+/+ 14.0 ± 1.7, n = 9 vs. A1AR−/− 15.3 ± 1.9 μL min−1g−1 bw). Diabetic animals had a similar tendency to develop interstitial fibrosis, whereas the glomerular volume was similar in both genotypes, and unaltered by diabetes.

    Conclusions: This study shows that the A1AR−/− mice develop diabetes-induced glomerular hyperfiltration, demonstrating that the TGF mechanism is not the major cause of the development of hyperfiltration. Furthermore, the hyperfiltration in the present study was not related to alterations in the glomerular filtration area.

1 - 6 of 6
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