Fregly M J, Rowland N E
Brain Res Bull. 1986 Mar;16(3):407-14. doi: 10.1016/0361-9230(86)90064-x.
Water intake, induced by subcutaneous (SC) administration of angiotensin II (AII, 200 micrograms/kg), isoproterenol (25 micrograms/kg), 5-hydroxytryptophan (25 mg/kg), and bethanechol (8 mg/kg), was reduced completely to control level by administration of either an intragastric (IG) or intraperitoneal (IP) load of distilled water (3% of body weight) prior to administration of the dipsogen. A similar load of isotonic saline given by both the IG and IP routes was either ineffective or only partially effective in reducing the dipsogenic response. The similar effectiveness of IP and IG loads of water in inhibiting the responsiveness to administration of dipsogenic agents argues against a gastrointestinal mechanism as an integral part of the feedback process limiting water intake in the rat. In addition, the lack of a significant effect of similar IP and IG loads of saline suggests that stretch of either the gastrointestinal or intraperitoneal spaces is not an important factor in the inhibition observed. A possibility exists that osmotic dilution, as a result of the water load, may play a role in the feedback inhibition of the drinking responses to the dipsogenic agents used in these studies, even though the responses were mediated via the AII receptor pathway rather than the osmoreceptor pathway.
通过皮下注射血管紧张素II(AII,200微克/千克)、异丙肾上腺素(25微克/千克)、5-羟色氨酸(25毫克/千克)和氨甲酰甲胆碱(8毫克/千克)诱导的饮水行为,在给予致渴剂之前通过胃内(IG)或腹腔内(IP)给予蒸馏水(体重的3%)可完全降低至对照水平。通过IG和IP途径给予等渗盐水的类似负荷在降低致渴反应方面无效或仅部分有效。IP和IG给予水负荷在抑制对致渴剂给药反应方面的相似有效性表明,胃肠道机制并非限制大鼠饮水的反馈过程的一个组成部分。此外,IP和IG给予盐水的类似负荷缺乏显著效果表明,胃肠道或腹腔空间的扩张不是观察到的抑制作用的重要因素。尽管这些反应是通过AII受体途径而非渗透压感受器途径介导的,但水负荷导致的渗透稀释可能在这些研究中使用的致渴剂饮水反应的反馈抑制中起作用。