Search: WFRF:(Carlström Mattias) >
Superoxide Dismutas...
-
Carlström, MattiasKarolinska Institutet,Uppsala universitet,Institutionen för medicinsk cellbiologi
(author)
Superoxide Dismutase 1 Limits Renal Microvascular Remodeling and Attenuates Arteriole and Blood Pressure Responses to Angiotensin II via Modulation of Nitric Oxide Bioavailability
- Article/chapterEnglish2010
Publisher, publication year, extent ...
Numbers
-
LIBRIS-ID:oai:DiVA.org:uu-140952
-
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-140952URI
-
https://doi.org/10.1161/HYPERTENSIONAHA.110.159301DOI
-
http://kipublications.ki.se/Default.aspx?queryparsed=id:121720348URI
Supplementary language notes
-
Language:English
-
Summary in:English
Part of subdatabase
Classification
-
Subject category:ref swepub-contenttype
-
Subject category:art swepub-publicationtype
Notes
-
Oxidative stress is associated with vascular remodeling and increased preglomerular resistance that are both implicated in the pathogenesis of renal and cardiovascular disease. Angiotensin II induces superoxide production, which is metabolized by superoxide dismutase (SOD) or scavenged by NO. We investigated the hypothesis that SOD1 regulates renal microvascular remodeling, blood pressure, and arteriolar responsiveness and sensitivity to angiotensin II using SOD1-transgenic (SOD1-tg) and SOD1-knockout (SOD1-ko) mice. Blood pressure, measured telemetrically, rose more abruptly during prolonged angiotensin II infusion in SOD1-ko mice. The afferent arteriole media: lumen ratios were reduced in SOD1-tg and increased in SOD1-ko mice. Afferent arterioles from nontreated wild types had graded contraction to angiotensin II (sensitivity: 10(-9) mol/L; responsiveness: 40%). Angiotensin II contractions were less sensitive (10(-8) mol/L) and responsive (14%) in SOD1-tg but more sensitive (10(-13) mol/L) and responsive (89%) in SOD1-ko mice. Arterioles from SOD1-ko had 4-fold increased superoxide formation with angiotensin II at 10(-9) mol/L. N-G-nitro-L-arginine methyl ester reduced arteriole diameter of SOD1-tg and enhanced angiotensin II sensitivity and responsiveness of wild-type and SOD1-tg mice to the level of SOD1-ko mice. SOD mimetic treatment with Tempol increased arteriole diameter and normalized the enhanced sensitivity and responsiveness to angiotensin II of SOD1-ko mice but did not affect wild-type or SOD1-tg mice. Neither SOD1 deficiency nor overexpression was associated with changes in nitrate/nitrite excretion or renal mRNA expression of NO synthase, NADPH oxidase, or SOD2/SOD3 isoforms and angiotensin II receptors. In conclusion, SOD1 limits afferent arteriole remodeling and reduces sensitivity and responsiveness to angiotensin II by reducing superoxide and maintaining NO bioavailability. This may prevent an early and exaggerated blood pressure response to angiotensin II.
Subject headings and genre
-
afferent arterioles
-
CuZnSOD
-
hypertension
-
ICSOD
-
oxidative stress
-
superoxide
-
SOD1
-
kidney
-
MEDICINE
-
MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
-
Lai, En YinUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)enlai087
(author)
-
Ma, ZufuUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)zufma109
(author)
-
Steege, Andreas
(author)
-
Patzak, Andreas
(author)
-
Eriksson, Ulf J.Uppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)ulfjerik
(author)
-
Lundberg, Jon O.Karolinska Institutet
(author)
-
Wilcox, Christopher S.
(author)
-
Persson, A. Erik G.Uppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)erikpers
(author)
-
Uppsala universitetInstitutionen för medicinsk cellbiologi
(creator_code:org_t)
Related titles
-
In:Hypertension56:5, s. 907-9130194-911X1524-4563
Internet link
Find in a library
To the university's database