Lal J, Atkinson J
Arch Int Pharmacodyn Ther. 1985 Dec;278(2):273-91.
This paper examined whether drinking elicited by morphine is dependent upon an intact renin-angiotensin system. Bilateral nephrectomy, carried out one day prior to administration of morphine, completely abolished morphine-induced water intake, pointing to involvement of the kidneys in the dipsogenic effect of morphine. Plasma and renal renin depletion were induced by the clipping of one renal artery followed, one month later, by removal of the clipped kidney. In such renin-depleted rats with subnormal plasma renin levels, morphine and isoprenaline-induced water intakes were linearly related to pre-injection basal plasma renin level. Such a relationship was not found in rats with normal renin levels. These results pointed to the existence of a permissive interaction between morphine and the renin-angiotensin system. Captopril, an inhibitor of the angiotensin converting enzyme, increased morphine-induced water intake. We interpreted this drinking response as being the sum of morphine-induced drinking (following a permissive interaction between morphine and circulating angiotensin I or renin) and captopril-induced drinking (following a captopril-induced increase in circulating renin and angiotensin I levels). The competitive antagonist of angiotensin II, saralasin, had no effect on morphine-induced drinking. This result pointed once again to a permissive interaction between morphine and circulating angiotensin I or renin.
本文研究了吗啡引起的饮水是否依赖于完整的肾素 - 血管紧张素系统。在给予吗啡前一天进行双侧肾切除术，可完全消除吗啡诱导的水摄入，这表明肾脏参与了吗啡的致渴作用。通过夹闭一侧肾动脉，一个月后切除夹闭侧肾脏来诱导血浆和肾脏肾素耗竭。在这种血浆肾素水平低于正常的肾素耗竭大鼠中，吗啡和异丙肾上腺素诱导的水摄入与注射前基础血浆肾素水平呈线性相关。在肾素水平正常的大鼠中未发现这种关系。这些结果表明吗啡与肾素 - 血管紧张素系统之间存在一种允许性相互作用。血管紧张素转换酶抑制剂卡托普利增加了吗啡诱导的水摄入。我们将这种饮水反应解释为吗啡诱导饮水（在吗啡与循环中的血管紧张素I或肾素之间存在允许性相互作用之后）和卡托普利诱导饮水（在卡托普利诱导循环中的肾素和血管紧张素I水平升高之后）的总和。血管紧张素II的竞争性拮抗剂沙拉新对吗啡诱导的饮水没有影响。这一结果再次表明吗啡与循环中的血管紧张素I或肾素之间存在允许性相互作用。
