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缓激肽在血管紧张素转换酶抑制的新生儿血流动力学效应中的作用。

The role of bradykinin in neonatal hemodynamic effects of ACE inhibition.

作者信息

Tóth-Heyn P, Thonney Viani M, Guignard J

机构信息

Service de Pédiatrie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

出版信息

Biol Neonate. 1999 Dec;76(6):389-92. doi: 10.1159/000014183.

Abstract

Angiotensin-converting enzyme (ACE) inhibitors exert their effects by inhibiting angiotensin II (AII) production, but also by inhibiting bradykinin (BK) degradation. In order to clarify whether BK is involved in the systemic effects of ACE inhibition in the newborn period, we investigated the effect of perindoprilat (20 microgram/kg i.v.) in newborn rabbits, with or without the blockade of BK beta(2)-receptors (Hoe 140, 300 microgram/kg s.c.). The bolus infusion of perindoprilat resulted in a marked fall in mean arterial blood pressure (MBP) and a slight decrease in heart rate. BK receptor blockade had no effect on the perindoprilat-induced hypotension but the negative chronotropic effect of ACE inhibition was partly prevented by pretreatment with Hoe 140. We therefore conclude that BK is not involved in neonatal blood pressure regulation but that the ACE inhibition-induced neonatal bradycardia is at least partly BK- mediated.

摘要

血管紧张素转换酶(ACE)抑制剂通过抑制血管紧张素II(AII)的产生发挥作用,但也通过抑制缓激肽(BK)的降解起作用。为了阐明BK是否参与新生儿期ACE抑制的全身效应,我们研究了培哚普利拉(20微克/千克静脉注射)对新生兔的影响,无论是否阻断BKβ2受体(Hoe 140,300微克/千克皮下注射)。推注培哚普利拉导致平均动脉血压(MBP)显著下降,心率略有降低。BK受体阻断对培哚普利拉诱导的低血压没有影响,但ACE抑制的负性变时作用部分被Hoe 140预处理所预防。因此,我们得出结论,BK不参与新生儿血压调节,但ACE抑制诱导的新生儿心动过缓至少部分是由BK介导的。

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