Elevated levels of endothelin-1 and prostaglandin E2 and their effect on nitric oxide generation in placental tissue from neonatal streptozotocin-induced diabetic rats

被引：17

作者：

Capobianco, E ^{[1
]}

Jawerbaum, A ^{[1
]}

White, V ^{[1
]}

Pustovrh, C ^{[1
]}

Sinner, D ^{[1
]}

Gonzalez, ET ^{[1
]}

机构：

[1] Consejo Nacl Invest Cient & Tecn, Ctr Estudios Farmacol & Bot, RA-1414 Buenos Aires, DF, Argentina

来源：

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2003年 / 68卷 / 03期

关键词：

D O I：

10.1016/S0952-3278(02)00274-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Endothelin-1 (ET-1), nitric oxide (NO) and prostaglandin E-2 (PGE(2)) are regulators of feto-placental hemodynamics. In this study we explore the inter-regulatory pathways that modulate the levels of these vasoactive agents in control and neonatal streptozotocin-induced (n-stz) diabetic rat placenta. ET-1 levels are increased in diabetic placenta when compared to controls (P<0.001), and are strongly reduced by an NO synthase inhibitor (P<0.001). PGE(2) production is increased in diabetic placenta when compared to controls (P<0.01), but these levels are not modulated by ET-1. NO levels, similar in control and in diabetic placenta, are not influenced by PGE(2), but they are negatively modulated by ET-1 in both control (P<0.05) and diabetic (P<0.01) placenta. We conclude that rat placental ET-1 inhibits NO levels but does not modify PGE(2) concentrations. The elevated levels of ET-1 and PGE(2) in diabetic placenta, potent vasoconstrictors of placental vasculature, are probably related to the induction of placental insufficiency and fetal hypoxia in this pathology. (C) 2003 Elsevier Science Ltd. All rights reserved.

引用

页码：225 / 231

页数：7

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