Fregly M J, Kelleher D L, Greenleaf J E
Brain Res Bull. 1981 Dec;7(6):661-4. doi: 10.1016/0361-9230(81)90114-3.
The dipsogenic responses of female rats to administration of angiotensin II (150 micrograms/kg b.w., IP), pilocarpine (3 mg/kg IP), hypertonic saline (1 M NaCl solution, 1% b.w.), and a 24 hour dehydration were attenuated by acute IP administration of graded doses of the central and peripheral alpha 2-adrenergic agonist, clonidine. For all treatments except dehydration, clonidine inhibited significantly the dipsogenic response at the lowest dose used (6 micrograms/kg, IP). The first significant effect on dehydration-induced drinking required approximately a 4 fold higher dose (25 micrograms/kg, IP). Attenuation of the response to these dipsogenic stimuli by clonidine, suggests that its ability to stimulate alpha-adrenergic receptors centrally may play an important role in its dipsogenic inhibitory activity.
雌性大鼠对静脉注射血管紧张素II(150微克/千克体重,腹腔注射)、毛果芸香碱(3毫克/千克腹腔注射)、高渗盐水(1M NaCl溶液,1%体重)以及24小时脱水的饮水反应,可通过腹腔注射不同剂量的中枢和外周α2 -肾上腺素能激动剂可乐定而减弱。除脱水外,对于所有处理,可乐定在所用最低剂量(6微克/千克,腹腔注射)时即可显著抑制饮水反应。对脱水诱导饮水的首个显著作用所需剂量约高4倍(25微克/千克,腹腔注射)。可乐定对这些致渴刺激反应的减弱表明,其在中枢刺激α -肾上腺素能受体的能力可能在其抑制饮水活性中起重要作用。