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肾素-血管紧张素系统和利钠肽系统在肺血管系统中的作用。

The role of the renin-angiotensin and natriuretic peptide systems in the pulmonary vasculature.

作者信息

Cargill R I, Lipworth B J

机构信息

Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee, Scotland, UK.

出版信息

Br J Clin Pharmacol. 1995 Jul;40(1):11-8. doi: 10.1111/j.1365-2125.1995.tb04528.x.

Abstract
  1. The role of vasoactive peptide systems in the pulmonary vasculature has been studied much less extensively than systemic vascular and endocrine effects. The current understanding of the role of the renin-angiotensin (RAS) and natriuretic peptide systems (NPS) in the pulmonary circulation is therefore reviewed. 2. Plasma concentrations of angiotensin II, the main vasoactive component of the RAS, are elevated in pulmonary hypertension and may interact with hypoxaemia to cause further pulmonary vasoconstriction. Pharmacological manipulation of angiotensin II can attenuate hypoxic pulmonary vasoconstriction but larger studies are needed to establish the efficacy of this therapeutic strategy in established pulmonary hypertension. 3. Although all the known natriuretic peptides, ANP, BNP and CNP are elevated in cor pulmonale, only ANP and BNP appear to have pulmonary vasorelaxant activity in humans. ANP and BNP can also attenuate hypoxic pulmonary vasoconstriction, suggesting a possible counter-regulatory role for these peptides. Inhibition of ANP/BNP metabolism by neutral endopeptidase has been shown to attenuate development of hypoxic pulmonary hypertension but this property has not been tested in humans. 4. It is also well established that there are potentially important endocrine and systemic circulatory interactions between the RAS and NPS. This also occurs in the pulmonary circulation and in humans, where at least BNP acts to attenuate angiotensin II induced pulmonary vasoconstriction. This interaction may be particularly relevant as a mechanism to counter-regulate overactivity of the RAS.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 与血管活性肽系统在体循环血管和内分泌方面的作用相比,其在肺血管系统中的作用研究得较少。因此,本文对肾素 - 血管紧张素系统(RAS)和利钠肽系统(NPS)在肺循环中的作用的当前认识进行综述。2. 血管紧张素II是RAS的主要血管活性成分,其血浆浓度在肺动脉高压时升高,并且可能与低氧血症相互作用导致进一步的肺血管收缩。对血管紧张素II进行药理调控可减弱低氧性肺血管收缩,但需要更大规模的研究来确定这种治疗策略在已确诊的肺动脉高压中的疗效。3. 虽然在肺心病中所有已知的利钠肽,即心房钠尿肽(ANP)、脑钠肽(BNP)和C型钠尿肽(CNP)均升高,但在人类中似乎只有ANP和BNP具有肺血管舒张活性。ANP和BNP也可减弱低氧性肺血管收缩,提示这些肽可能具有一种反调节作用。中性内肽酶对ANP/BNP代谢的抑制已被证明可减弱低氧性肺动脉高压的发展,但这一特性尚未在人类中进行测试。4. 同样公认的是,RAS和NPS之间存在潜在重要的内分泌和体循环相互作用。这在肺循环中以及在人类中也会发生,其中至少BNP可减弱血管紧张素II诱导的肺血管收缩。这种相互作用作为一种对抗RAS过度激活的机制可能特别重要。(摘要截选至250词)

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