Mercer P F, Mogenson G J, Paquette S Y
Can J Physiol Pharmacol. 1978 Apr;56(2):252-9. doi: 10.1139/y78-037.
Sodium intake and sodium output were measured in rats before and after lesioning of the anterior hypothalamus. Both parameters were lower than control rats following the lesioning procedure. When an amount of sodium was given orally to these lesioned rats to make up the deficit in sodium intake, no difference was found in sodium intake or output between the rats with lesions and normal rats. Rats with anterior hypothalamic lesions were able to increase their sodium intake following a period of sodium deprivation or adrenalectomy. When presented with concentrations of sodium chloride ranging between 0.9 and 2.5% rats with lesions decreased their intake of sodium in a manner similar to control rats except that the level of intake in the lesioned rats was lower for all concentrations. Control rats and those with lesions were not different in their intakes of KC1 solutions. These findings suggest that the anterior hypothalamus is important in setting the absolute intakes of sodium but does not interfere with the control mechanisms regulating the sodium intake.
在损毁大鼠下丘脑前部前后，分别测量其钠摄入量和钠排出量。损毁手术后，这两个参数均低于对照大鼠。当给这些损毁大鼠口服一定量的钠以弥补钠摄入不足时，损毁大鼠与正常大鼠在钠摄入量或排出量上未发现差异。下丘脑前部损毁的大鼠在经历一段时间的钠缺乏或肾上腺切除后，能够增加其钠摄入量。当给予浓度在0.9%至2.5%之间的氯化钠时，损毁大鼠会以与对照大鼠相似的方式减少钠摄入量，只是在所有浓度下，损毁大鼠的摄入量水平较低。对照大鼠和损毁大鼠对氯化钾溶液的摄入量没有差异。这些发现表明，下丘脑前部在设定钠的绝对摄入量方面很重要，但不干扰调节钠摄入的控制机制。
