Oxidative stress and nitric oxide system in post-transplant hypertension

被引:0
作者
Calò, L
Marcon, R
Rigotti, P
Pagnin, E
Mennella, G
Spinello, M
Bonfante, L
Cantaro, S
D'Angelo, A
Semplicini, A
Antonello, A
机构
[1] Univ Padua, Dept Clin & Exptl Med, Med Clin 4, I-35128 Padua, Italy
[2] Univ Padua, Dept Med & Surg Sci, Div Nephrol, Padua, Italy
[3] Univ Padua, Dept Med & Surg Sci, Div Gen Surg, Padua, Italy
关键词
nitric oxide; oxidative stress; post-transplant hypertension;
D O I
暂无
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: CsA-induced endothelial dysfunction and CsA-induced hypertension have been attributed to CsA effects on the endothelial-derived factors controlling vasomotor tone, but the mechanisms responsible are unclear. Endothelial nitric oxide (NO) is known to maintain a state of basal vasodilation and recently a NO mediated counterregulatory mechanism protective from CsA-induced vasoconstriction has been suggested. Patients and methods: Our study evaluates ecNOS gene status and NO metabolites in kidney transplanted patients under chronic CsA treatment with CsA-induced hypertension, Since CsA increases superoxide production, which metabolizes NO, plasma hydroperoxides and peroxynitrite were also evaluated as index of the presence of "oxidative stress". Results: Quantification of monocyte ecNOS mRNA and NO metabolites plasma level from patients and control subjects (C) demonstrated NO system up regulation in patients notwithstanding hypertension. The mean ecNOS to beta-actin ratio was 2.00 +/- 0.87 vs 0.29 +/- 0.08 in C, p < 0.04. NO metabolite plasma level was 30.03 +/- 9.62 mM vs 9.37 +/- 3.86. p < 0.001. Hydroperoxides were also increased in patients: 3.6 +/- 1.6 i.a.u. vs 1.4 +/- 0.. p < 0.007 (from cholesterol esters) and 10.8 +/- 6.6 vs 1.5 +/- 0.9, p < 0.008 (from triglycerides) as well as peroxynitrite plasma level: 0.36 +/- 0.14 mM/L vs undetectable in C. Conclusions: This study confirms a NO system up-regulation in transplanted patients. However. the counterregolatory system to CsA-induced vasoconstriction. could be cancelled by CsA induced superoxide and free radicals production which, increasing NO metabolism could contribute to CsA induced vasoconstriction and hypertension.
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页码:B6 / B7
页数:2
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