EVIDENCE FOR A DUAL CENTRAL ROLE FOR ANGIOTENSIN IN WATER AND SODIUM INTAKE
EVIDENCE FOR A DUAL CENTRAL ROLE FOR ANGIOTENSIN IN WATER AND SODIUM INTAKE
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DOI：
10.1038/250733a0
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发表时间：
1974-01-01
期刊：
影响因子：
64.8
通讯作者：
FISHER, AE
中科院分区：
文献类型：
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作者：
BUGGY, J;FISHER, AE
血管紧张素II通过血管内注入或注射到哺乳动物的特定脑区，可诱导短潜伏期水摄入1,2。但如果有人问为什么会这样，以及这些数据是否反映了真实的生理行为，就会出现概念上的困难。例如，血管紧张素是一种压力激素，是由肾基肾素在应对低血压和低血容量等挑战时形成的。水摄入本身并不是对这种挑战的适应性反应，因为大多数摄入的水分布在细胞内，不会缓解血管危机。对低血压或低血容量的适应性反应包括摄入等渗混合液体，因为这将最迅速有效地增加血管容量。事实上，低血容量确实会导致对等渗盐水的偏好立即增加，并延迟（6-10小时）接受令人不快的高渗盐溶液8,9。但是，血管紧张素可能作为钠摄入的快速和直接的促进剂（除了通过刺激醛固酮释放缓慢和间接的作用）尚未报道，一些证据表明血管紧张素可能在调节小鼠钠摄入方面没有任何重要作用10 - 12。
ANGIOTENSIN II induces short-latency water intake when infused intravascularly or injected into certain brain regions of mammals1,2. But conceptual difficulties arise if one asks why this should be so, and whether the data reflect real physiological actions. For example, angiotensin is a pressor hormone formed from kidney-based renin in response to challenge such as hypotension and hypovolaemia3–7. Water ingestion, in itself, is not an adaptive response to such challenges, since most ingested water is distributed intracellularly and will not relieve a vascular crisis. An adaptive response to hypotension or hypovolaemia would involve ingestion of an isotonic mix of fluids, since this would most rapidly and effectively increase vascular volume. In fact, hypovolaemia does result in an immediate increase in preference for isotonic saline over water and a delayed (6–10 h) acceptance of unpalatable hypertonic salt solutions8,9. But, a possible involvement of angiotensin as a rapid and direct facilitator of sodium intake (apart from a slow and indirect role through stimulation of aldosterone release) has not yet been reported and some evidence suggests that angiotensin may not play any significant role in regulating sodium intake in the rat10–12.