Rouah-Rosilio M, Orosco M, Nicolaidis S
Neurobiologie des Régulations, URA CNRS 637, Collège de France, Paris.
Physiol Behav. 1994 May;55(5):811-6. doi: 10.1016/0031-9384(94)90064-7.
There are two mechanisms leading to an enhancement of salt intake: one is induced by a sodium deficit and the other is need-free. The serotonin involvement in need-induced and/or need-free sodium appetite is interesting to consider because related drugs are already used against another cardiovascular risk factor, obesity. The effect of dexfenfluramine (1.5 or 3 mg/kg), an anorectic drug enhancing 5-HT transmission, and of metergoline (2 or 4 mg/kg), a 5-HT antagonist, was assessed in need-induced (depletion-induced), subsequent need-free, and spontaneous sodium appetite. Dexfenfluramine (3 mg/kg) decreased by 75% to 90% the depletion-induced intake of an aversive 3% NaCl solution, as well as the spontaneous intake of a less aversive 1.8% NaCl solution. Water intake was not diminished under these conditions. Metergoline significantly increased salt intake in need-free conditions in rats with either a history of three previous depletions or not. These results confirm the involvement of serotonin in sodium appetite and extend this involvement to both need-induced (natriorexis) and need-free (natriophilia) conditions. The metergoline experiments also suggest that 5-HT exerts a tonic inhibition on salt intake.
一种是由钠缺乏引起的，另一种是无需求性的。血清素参与需求诱导型和/或无需求型钠食欲值得研究，因为相关药物已被用于对抗另一种心血管危险因素——肥胖。评估了食欲抑制剂右芬氟拉明（1.5或3毫克/千克）（一种增强5-羟色胺传递的药物）和麦角林（2或4毫克/千克）（一种5-羟色胺拮抗剂）对需求诱导型（耗竭诱导型）、随后的无需求型和自发性钠食欲的影响。右芬氟拉明（3毫克/千克）使耗竭诱导的3%厌恶氯化钠溶液摄入量以及1.8%较低厌恶度氯化钠溶液的自发性摄入量减少了75%至90%。在这些条件下，水的摄入量并未减少。对于有过三次先前耗竭史或无此历史的大鼠，麦角林在无需求条件下显著增加了盐摄入量。这些结果证实了血清素参与钠食欲，并将这种参与扩展到需求诱导型（钠摄取亢进）和无需求型（嗜钠）条件。麦角林实验还表明，5-羟色胺对盐摄入量有持续性抑制作用。
