Stanek B, Bruckner U, Silberbauer K
J Hypertens Suppl. 1985 Nov;3(2):S129-31.
The activation of the renin-angiotensin system that occurs during the development of congestive heart failure (CHF) may be accompanied by continued secretion of vasopressin (AVP) in response to non-osmotic stimuli. Increased supine plasma AVP levels (by radio-immunoassay) were found in 31 patients with moderate to severe CHF (11.49 +/- 1.00 pg/ml s.e.m.) 24 h after the last diuretic dose, which correlated with plasma renin activity (PRA) (r = 0.37, P less than 0.05). However, acute inhibition of converting enzyme with captopril did not decrease plasma AVP levels (14.9 +/- 3.9 versus 14.0 +/- 2.8 pg/ml, n = 8). Indeed, in six out of eight patients, plasma AVP actually increased following captopril - presumably secondary to haemodynamic changes. Readministration of captopril after 4 months of captopril treatment, 12 h after the last dose, again did not change AVP levels (9.58 +/- 1.2 versus 13.1 +/- 1.9 pg/ml), whereas changes in haemodynamics, PRA and angiotensin II were as expected and similar to the first test. These results suggest that the acute haemodynamic action of captopril in CHF is not mediated via suppression of vasopressin, although in some patients with non-osmotic vasopressin, excess activation of the renin-angiotensin-aldosterone system might constitute a factor.
充血性心力衰竭（CHF）发展过程中发生的肾素 - 血管紧张素系统激活，可能伴随着血管加压素（AVP）因非渗透性刺激而持续分泌。在31例中重度CHF患者中，末次使用利尿剂24小时后，通过放射免疫测定发现仰卧位血浆AVP水平升高（11.49±1.00 pg/ml标准误），这与血浆肾素活性（PRA）相关（r = 0.37，P＜0.05）。然而，用卡托普利急性抑制转换酶并没有降低血浆AVP水平（14.9±3.9对14.0±2.8 pg/ml，n = 8）。实际上，在8例患者中有6例，卡托普利治疗后血浆AVP实际上升高了 - 可能继发于血流动力学变化。卡托普利治疗4个月后，末次给药12小时后再次给予卡托普利，同样没有改变AVP水平（9.58±1.2对13.1±1.9 pg/ml），而血流动力学、PRA和血管紧张素II的变化如预期且与首次试验相似。这些结果表明，卡托普利在CHF中的急性血流动力学作用不是通过抑制血管加压素介导的，尽管在一些非渗透性血管加压素分泌过多的患者中，肾素 - 血管紧张素 - 醛固酮系统的过度激活可能是一个因素。
