Levens N R
Am J Physiol. 1984 Jun;246(6 Pt 1):G700-9. doi: 10.1152/ajpgi.1984.246.6.G700.
In the pentobarbital sodium-anesthetized rat, dehydration for 24 h increased ion and water absorption from the jejunum. Dehydration also elevated plasma concentrations of angiotensin peptides and plasma renin activity but did not significantly alter plasma aldosterone concentrations. Infusion of tyramine, norepinephrine, and angiotensin II (AII) also stimulated jejunal absorption in a manner similar to dehydration. The elevation of jejunal absorption in response to dehydration is totally inhibited by the converting enzyme inhibitor captopril and the angiotensin receptor antagonist [lle7]AIII. Thus, increased jejunal absorption following dehydration is mediated by the renin-angiotensin system and is not secondary to either aldosterone or to antidiuretic hormone release. Further experiments demonstrated that the increase in jejunal absorption in response to dehydration was unaffected by propranolol but was totally abolished by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII stimulates jejunal absorption by enhancing transepithelial transport processes and/or by altering the balance of Starling forces governing fluid absorption across enteric capillaries. Angiotensin thus appears to be a physiologically important mediator of jejunal absorption in states characterized by extracellular volume depletion.
在戊巴比妥钠麻醉的大鼠中,脱水24小时可增加空肠对离子和水的吸收。脱水还会提高血浆中血管紧张素肽的浓度和血浆肾素活性,但不会显著改变血浆醛固酮浓度。注入酪胺、去甲肾上腺素和血管紧张素II(AII)也会以类似于脱水的方式刺激空肠吸收。脱水引起的空肠吸收增加完全被转化酶抑制剂卡托普利和血管紧张素受体拮抗剂[Ile7]AIII抑制。因此,脱水后空肠吸收增加是由肾素-血管紧张素系统介导的,并非继发于醛固酮或抗利尿激素释放。进一步的实验表明,脱水引起的空肠吸收增加不受普萘洛尔的影响,但完全被酚妥拉明、哌唑嗪和外周交感神经切除术消除。有人提出,AII通过增强跨上皮转运过程和/或通过改变控制肠毛细血管间液体吸收的Starling力平衡来刺激空肠吸收。因此,在以细胞外液量减少为特征的状态下,血管紧张素似乎是空肠吸收的一种重要生理介质。