Abstract：
:Endothelin (ET-1) is chronically elevated in diabetes. However, role of ET-1 in increased oxidative stress in type 2 diabetes is less clear. This study tested the hypotheses that: 1) oxidative stress markers are increased and total antioxidant capacity is decreased in diabetes, and 2) activation of ET(A) receptors mediates oxidative stress whereas ET(B) receptors display opposing effects. Plasma total antioxidant status (TAS) and 8-isoprostane (8-iso PGF(2alpha)) as well as total nitrotyrosine levels in mesenteric resistance vessels were measured in control Wistar and diabetic Goto-Kakizaki (GK) rats (n=5-10) treated with vehicle, ET(A) antagonist (atrasentan, 5 mg/kg/day), or ET(B) receptor antagonist (A-192621, 15 or 30 mg/kg/day, low and high dose, respectively) for 4 weeks. 8-iso PGF(2alpha) (pg/ml) levels were significantly higher in low dose A-192621 treatment groups of control and diabetic rats than in atrasentan or high-dose A-192621 treated groups. Protein nitration was increased in diabetes and ET(A) receptor antagonism prevented this increase. TAS levels were similar in all experimental groups. Thus, ET-1 contributes to oxidative stress in type 2 diabetes and ET receptor antagonism with atrasentan or A-192612 displays differential effects depending on dose and receptor subtype.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Elgebaly MM,Portik-Dobos V,Sachidanandam K,Rychly D,Malcom D,Johnson MH,Ergul Adoi
10.1016/j.vph.2007.05.006subject
Has Abstractpub_date
2007-08-01 00:00:00pages
125-30issue
2-3eissn
1537-1891issn
1879-3649pii
S1537-1891(07)00095-Xjournal_volume
47pub_type
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