Sodium appetite decreased by central angiotensin blockade
Sodium appetite decreased by central angiotensin blockade
复制标题
中枢血管紧张素阻断可降低钠食欲
DOI：
10.1016/0031-9384(84)90187-2
复制
发表时间：
1984
影响因子：
2.9
通讯作者：
J. Jonklaas
中科院分区：
文献类型：
--
作者：
J. Buggy;J. Jonklaas
体内水分和电解质的紊乱，如钠耗竭或血容量不足，触发钠食欲，是肾素-血管紧张素系统的有效激活剂。在没有体液实际不足的情况下，血管紧张素注射足以刺激钠摄入增加。为了评估血管紧张素是否是体液急性变化诱导的钠食欲的重要介质，在中枢或外周血管紧张素阻断期间检查大鼠的钠摄入量。通过脑室内（ICVT）注射类似物拮抗剂saralasin对血管紧张素受体进行中枢阻滞，可降低（但不能消除）聚乙二醇诱导的低血容量或葡萄糖透析导致的钠耗竭后的钠摄入量。相反，口服活性卡托普利外周阻断血管紧张素转换酶增强，而不是降低钠食欲和刺激钠耗竭后的水摄入。这种增加的水和盐的摄入量后，外周抑制转换酶逆转，然而，并发的血管紧张素受体的中枢阻滞。这些数据支持血管紧张素参与与体液急性改变相关的钠食欲的假设。此外，大脑是血管紧张素对钠食欲产生影响的部位。虽然不排除脑源性血管紧张素的参与，但外周阻断转换酶后钠食欲的变化表明，来自肾肾素的循环血管紧张素可能与调节钠食欲的中枢血管紧张素受体相互作用。
Disturbances in body water and electrolytes that trigger sodium appetite, such as sodium depletion or hypovolemia, are potent activators of the renin-angiotensin system. In the absence of an actual deficit in body fluids, angiotensin injections are adequate to stimulate increased sodium ingestion. To assess whether angiotensin is a significant mediator of sodium appetite induced by acute alterations in body fluids, sodium intake was examined in rats during central or peripheral angiotensin blockade. Central blockade of angiotensin receptors by intracerebroventricular (ICVT) injection of the analogue antagonist saralasin decreased (but did not eliminate) sodium intake after polethylene glycol-induced hypovolemia or sodium depletion resulting from dialysis against glucose. Conversely, peripheral blockade of angiotensin converting exzyme with orally active captopril potentiated rather than decreased sodium appetite and stimulated water intake after sodium depletion. This increased water and salt intake after peripheral inhibition of converting enzyme was reversed, however, by concurrent central blockade of angiotensin receptors. These data support the hypothesis that angiotensin participates in sodium appetite associated with acute alteration in body fluids. Furthermore, the brain is the site at which angiotensin exerts its influence on sodium appetite. While the involvement of angiotensin of brain origin is not ruled out, the change in sodium appetite after peripheral blockade of converting enzyme suggests that circulating angiotensin derived from renal renin may interact with central angiotensin receptors regulating sodium appetite.