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SOD1-Deficiency Cau...
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Carlström, MattiasKarolinska Institutet,Uppsala universitet,Integrativ Fysiologi
(author)
SOD1-Deficiency Causes Salt-Sensitivity and Aggravates Hypertension in Hydronephrosis
- Article/chapterEnglish2009
Publisher, publication year, extent ...
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American Physiological Society,2009
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-104360
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-104360URI
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https://doi.org/10.1152/ajpregu.90843.2008DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:118989477URI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Background: Hydronephrosis causes renal dysfunction and salt-sensitive hypertension, which is associated with NO-deficiency and abnormal tubuloglomerular feedback (TGF) response. We investigated the role of oxidative stress for salt-sensitivity and for hypertension in hydronephrosis. Methods: Hydronephrosis was induced in SOD1-transgenic (SOD1-tg), SOD1-deficient (SOD1-ko) and wild-type mice and in rats. In mice, telemetric measurements were performed during normal (0.7% NaCl) and high sodium (4% NaCl) diets and with chronic Tempol supplementation. 8-iso-prostaglandin-F2alpha (F2-IsoPs) and protein excretion profiles and histology were investigated. The acute effects of Tempol on blood pressure and TGF were studied in rats. Results: In hydronephrosis, wild-type mice developed salt-sensitive hypertension (114+/-1 to 120+/-2 mmHg) which was augmented in SOD1-ko (125+/-3 to 135+/-4 mmHg), but abolished in SOD1-tg (109+/-3 to 108+/-3 mmHg). SOD1-ko controls displayed salt-sensitive blood pressure (108+/-1 to 115+/-2 mmHg), which was not found in wild-types or SOD1-tg. Chronic Tempol treatment reduced blood pressure in SOD1-ko controls (-7 mmHg) and in hydronephrotic wild-types (-8 mmHg) and SOD1-ko mice (-16 mmHg), but had no effect on blood pressure in wild-type or SOD1-tg controls. SOD1-ko controls and hydronephrotic wild-type and SOD1-ko mice exhibited increased fluid excretion associated with increased F2-IsoPs and protein excretion. The renal histopathological changes found in hydronephrotic wild-types were augmented in SOD1-ko and diminished in SOD-tg mice. Tempol attenuated blood pressure and normalized TGF response in hydronephrosis (DeltaPSF: 15.2+/-1.2 to 9.1+/-0.6 mmHg, TP: 14.3+/-0.8 to 19.7+/-1.4 nl/min). Conclusion: Oxidative stress due to SOD1-deficiency causes salt-sensitivity and plays a pivotal role for the development of hypertension in hydronephrosis. Increased superoxide formation may enhance TGF response and thereby contribute to hypertension.
Subject headings and genre
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blood pressure
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CuZnSOD
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isoprostanes
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superoxide
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telemetry
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tempol
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tubuloglomerular feedback
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ureteral obstruction
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oxidative stress
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MEDICINE
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MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
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Brown, Russell DUppsala universitet,Integrativ Fysiologi
(author)
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Sällström, JohanUppsala universitet,Integrativ Fysiologi
(author)
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Larsson, ErikUppsala universitet,Institutionen för genetik och patologi(Swepub:uu)eriklars
(author)
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Zilmer, Mihkel
(author)
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Zabihi, ShellerUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)shzab676
(author)
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Eriksson, Ulf JUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)ulfjerik
(author)
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Persson, A Erik GUppsala universitet,Integrativ Fysiologi(Swepub:uu)erikpers
(author)
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Uppsala universitetIntegrativ Fysiologi
(creator_code:org_t)
Related titles
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In:American Journal of Physiology. Regulatory Integrative and Comparative Physiology: American Physiological Society297:1, s. R82-R920363-61191522-1490
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