Swales J D, Tange J D, Thurston H
Circ Res. 1975 Jul;37(1):96-100. doi: 10.1161/01.res.37.1.96.
The relationship between the vascular response. to angiotensin II and sodium balance was studied by measuring the volume of specific antiserum needed to block the pressor response to a standard dose of angiotensin II in rats. In normal rats, sodium depletion reduced the volume of antiserum required to prevent a pressor response to 50 ng of angiotensin II from 0.32 to 0.22 ml; sodium loading increased the volume required to 0.65 ml. After bilateral nephrectomy, there was a progressive increase in the antibody requirement to a maximum of 0.63 ml at 6 hours. At this stage, there was no change in the blocking requirement with sodium depletion by either pretreatment with a low-salt diet (0.60 ml) or peritoneal dialysis (0.62 ml). The pressor response to a 50-ng bolus of angiotensin II was closely correlated with the antibody requirement in all experiments (r equals plus 0.93). These observations indicate that sodium-induced changes in the vascular response to angiotensin II require the presence of kidney tissue. We suggest that such changes in response are mediated by alterations in vascular renin which generates angiotensin II at an arteriolar site that is not accessible to antibody molecules. This locally formed angiotensin II reduces the number of receptors free to respond to circulating angiotensin II and raises the threshold of the pressor response
通过测量阻断大鼠对标准剂量血管紧张素II的升压反应所需的特异性抗血清体积，研究了血管对血管紧张素II的反应与钠平衡之间的关系。在正常大鼠中，缺钠使预防对50 ng血管紧张素II的升压反应所需的抗血清体积从0.32 ml降至0.22 ml；钠负荷则使所需体积增加至0.65 ml。双侧肾切除术后，抗体需求量逐渐增加，在6小时时达到最大值0.63 ml。在此阶段，通过低盐饮食预处理（0.60 ml）或腹膜透析（0.62 ml）导致的缺钠并未使阻断需求量发生变化。在所有实验中，对50 ng血管紧张素II推注的升压反应与抗体需求量密切相关（r等于+0.93）。这些观察结果表明，钠诱导的血管对血管紧张素II反应的变化需要肾脏组织的存在。我们认为，这种反应变化是由血管肾素的改变介导的，血管肾素在抗体分子无法到达的小动脉部位生成血管紧张素II。这种局部形成的血管紧张素II减少了可对循环血管紧张素II作出反应的游离受体数量，并提高了升压反应的阈值。
