Arnolda L, McGrath B P, Johnston C I
Melbourne University Department of Medicine, Austin Hospital, Victoria Australia.
Cardiovasc Res. 1991 Jan;25(1):68-72. doi: 10.1093/cvr/25.1.68.
Vasopressin, like angiotensin, has both vasoconstrictor and fluid retaining properties and therefore may make an important contribution to the pathogenesis of low output congestive heart failure. The study aimed to examine the relative importance of the renin-angiotensin system and vasopressin in an animal model of heart failure.
The acute haemodynamic effects of vasopressin receptor blockade with a selective antagonist, d(CH2)5DAVP (AVPA) (30 micrograms.kg-1) and angiotensin converting enzyme inhibition with captopril (1 mg.kg-1) were compared. The effect of combined blockade (ie, vasopressin receptor antagonist + angiotensin converting enzyme inhibitor) was also examined.
Rabbits, 2.5-3.5 kg, with doxorubicin induced cardiomyopathy and heart failure (n = 20) were used. There were 15 controls.
Both AVPA and captopril produced significant increases in cardiac output (11% and 13% respectively) and falls in peripheral vascular resistance (21% and 17% respectively). Inhibition of the two vasoconstrictor systems was additive and resulted in a fall in peripheral vascular resistance to levels found in normal animals.
Vasopressin and angiotensin II make equal contributions to the raised peripheral vascular resistance observed in this model of heart failure. Vasopressin inhibition may be useful in the treatment of heart failure either alone or as an adjunct to angiotensin converting inhibition.
血管加压素与血管紧张素一样,兼具血管收缩和保液特性,因此可能在低输出量充血性心力衰竭的发病机制中发挥重要作用。本研究旨在探讨在心力衰竭动物模型中肾素 - 血管紧张素系统和血管加压素的相对重要性。
比较了选择性拮抗剂d(CH2)5DAVP(AVPA,30微克·千克⁻¹)阻断血管加压素受体和卡托普利(1毫克·千克⁻¹)抑制血管紧张素转换酶的急性血流动力学效应。还研究了联合阻断(即血管加压素受体拮抗剂 + 血管紧张素转换酶抑制剂)的效果。
使用体重2.5 - 3.5千克、由阿霉素诱导心肌病和心力衰竭的兔子(n = 20)。有15只对照兔子。
AVPA和卡托普利均使心输出量显著增加(分别为11%和13%),外周血管阻力下降(分别为21%和17%)。两种血管收缩系统的抑制作用具有相加性,导致外周血管阻力降至正常动物的水平。
在该心力衰竭模型中,血管加压素和血管紧张素II对升高的外周血管阻力起同等作用。抑制血管加压素可能单独用于治疗心力衰竭,或作为血管紧张素转换抑制的辅助手段。