Beuers U, Hertting G, Knepel W
Br J Pharmacol. 1982 Aug;76(4):579-85. doi: 10.1111/j.1476-5381.1982.tb09257.x.
1 The influence of the renin-angiotensin system on plasma beta-endorphin-like immunoreactivity (beta-EI) was investigated in the conscious rat by use of a radioimmunoassay for beta-endorphin without prior extraction.2 Intravenous infusion of angiotensin I, II or (des-1-Asp)angiotensin II (angiotensin III) caused a dose-dependent increase in plasma beta-EI, angiotensin III infusion being less effective than angiotensin I or II. The plasma adrenocorticotrophin (ACTH) levels too were elevated by angiotensin II. The receptor antagonist, saralasin, prevented the angiotensin II-induced beta-EI release as did dexamethasone pretreatment.3 Both the release of beta-EI and the pressor response to angiotensin I were abolished by the converting enzyme inhibitor, captopril (SQ 14225). In contrast, captopril did not affect the action of angiotensin II.4 In view of the appreciable cross-reactivity of beta-lipotropin (beta-LPH) in our assay, plasma beta-EI was analysed by Sephadex G-50 chromatography. In plasma extracts of angiotensin II-infused rats, immunoreactivity corresponding to human beta-endorphin comprised about 49% of the total immunoreactivity, whereas 51% co-migrated with human beta-LPH.5 The increase in plasma levels of beta-EI elicited by angiotensin II was diminished by about 35% in rats with a hereditary absolute lack of vasopressin (Brattleboro rats), when compared to normal rats.6 These results suggest that the renin-angiotensin system can stimulate the secretion of beta-LPH and beta-endorphin with ACTH from rat anterior pituitary. One link in mediating the response appears to be vasopressin. The physiological function remains to be defined.
1 通过使用无需预先提取的β-内啡肽放射免疫分析法,在清醒大鼠中研究了肾素-血管紧张素系统对血浆β-内啡肽样免疫反应性(β-EI)的影响。
2 静脉输注血管紧张素I、II或(去1-天冬氨酸)血管紧张素II(血管紧张素III)导致血浆β-EI呈剂量依赖性增加,血管紧张素III输注的效果低于血管紧张素I或II。血管紧张素II也使血浆促肾上腺皮质激素(ACTH)水平升高。受体拮抗剂沙拉新和地塞米松预处理一样,可阻止血管紧张素II诱导的β-EI释放。
3 转换酶抑制剂卡托普利(SQ 14225)消除了β-EI的释放以及对血管紧张素I的升压反应。相比之下,卡托普利不影响血管紧张素II的作用。
4 鉴于我们的分析中β-促脂素(β-LPH)有明显的交叉反应性,通过葡聚糖G-50柱色谱法分析血浆β-EI。在输注血管紧张素II的大鼠血浆提取物中,与人β-内啡肽相对应的免疫反应性约占总免疫反应性的49%,而51%与人类β-LPH共同迁移。
5 与正常大鼠相比,遗传性完全缺乏抗利尿激素的大鼠(布拉特洛维大鼠)中,血管紧张素II引起的血浆β-EI水平升高减少了约35%。
6 这些结果表明,肾素-血管紧张素系统可刺激大鼠垂体前叶分泌β-LPH、β-内啡肽和ACTH。介导该反应的一个环节似乎是抗利尿激素。其生理功能仍有待确定。