Montgomery A M, Burton M J
Psychopharmacology (Berl). 1986;89(2):192-7. doi: 10.1007/BF00310628.
Systemic administration of serotonin (5-hydroxytryptamine, 5-HT) to non-deprived rats increased saline (0.9%) consumption (5-HT hyperdipsia), without altering saline preference in two-bottle test. When sodium saccharin (0.1%) was the test solution 5-HT suppressed both consumption and preference. 5-HT saline hyperdipsia was blocked by pretreatment with an angiotensin I converting enzyme inhibitor (MK421) and mimicked by isoprenaline-induced stimulation of renin production; saccharin consumption and preference were unaffected by either drug. However, methysergide (a 5-HT antagonist) attenuated the effects of 5-HT on saccharin consumption and preference, thus confirming that these effects are mediated via peripheral 5-HT receptors. It is suggested that the effects of 5-HT on saline consumption are mediated via stimulation of the renin-angiotensin system, but its effects on saccharin consumption and preference are mediated by a separate mechanism at some point subsequent to peripheral 5-HT receptors.
对未禁食大鼠进行血清素（5-羟色胺，5-HT）的全身给药会增加其对生理盐水（0.9%）的消耗量（5-HT 引起的饮水过多），且在双瓶试验中不改变对生理盐水的偏好。当测试溶液为糖精钠（0.1%）时，5-HT 会抑制消耗量和偏好。5-HT 引起的生理盐水饮水过多可被血管紧张素 I 转换酶抑制剂（MK421）预处理所阻断，并可被异丙肾上腺素诱导的肾素分泌刺激所模拟；两种药物均不影响糖精的消耗量和偏好。然而，麦角新碱（一种 5-HT 拮抗剂）减弱了 5-HT 对糖精消耗量和偏好的影响，从而证实这些影响是通过外周 5-HT 受体介导的。研究表明，5-HT 对生理盐水消耗量的影响是通过刺激肾素-血管紧张素系统介导的，但其对糖精消耗量和偏好的影响是在外周 5-HT 受体之后的某个点由一种独立机制介导的。
