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[血管加压素拮抗剂]

[Vasopressin antagonists].

作者信息

de Groote P

机构信息

Service de cardiologie C, hôpital cardiologique, CHRU Lille, 59037 Lille.

出版信息

Arch Mal Coeur Vaiss. 2002 Feb;95 Spec 4(5 Spec 4):59-61.

Abstract

Vasopressin, like all the other neuro-hormonal systems, is activated in patients with cardiac insufficiency. Vasopressin attaches itself to two distinct specific receptors. It is through the intermediary of the renal V2 receptor, controlling the reabsorption of water by the collecting duct, that vasopressin finely regulates the blood osmolarity. The ubiquitous V1a receptor is essentially responsible for the vasoconstrictor effect of the hormone. Some specific antagonists for these two receptors have now been evaluated in various pathologies such as SIADH, cirrhosis or cardiac insufficiency. In this situation the mixed antagonists, anti-V1a-V2, seem more appropriate than the specific V1a or V2 receptor antagonists. The results of the first human studies are encouraging. The mixed antagonists reduce the pulmonary capillary pressure and increase diuresis and clearance of free water. But further studies are necessary to confirm these results and to demonstrate a reduction in morbidity and mortality before adding this class of medication to the therapeutic arsenal for our patients with cardiac insufficiency.

摘要

与所有其他神经激素系统一样,血管加压素在心脏功能不全患者中被激活。血管加压素与两种不同的特异性受体结合。血管加压素通过控制集合管对水重吸收的肾脏V2受体这一媒介,精细调节血液渗透压。普遍存在的V1a受体主要负责该激素的血管收缩作用。目前已在多种病症(如抗利尿激素分泌失调综合征、肝硬化或心脏功能不全)中对这两种受体的一些特异性拮抗剂进行了评估。在这种情况下,混合拮抗剂(抗V1a-V2)似乎比特异性V1a或V2受体拮抗剂更合适。首批人体研究结果令人鼓舞。混合拮抗剂可降低肺毛细血管压力,并增加利尿和自由水清除率。但在将这类药物添加到我们心脏功能不全患者的治疗手段之前,还需要进一步研究来证实这些结果,并证明其能降低发病率和死亡率。

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