Kiss A, Jezova D, Aguilera G
Developmental Endocrinology Branch, National Institute of, Child Health and Human Development, NIH, Bethesda, MD 20892.
Brain Res. 1994 Nov 7;663(1):84-92. doi: 10.1016/0006-8993(94)90465-0.
It has been previously shown that chronic water deprivation or hypertonic saline intake, osmotic stress models with concomitant decrease in food intake, decrease hypothalamic CRH mRNA levels and ACTH responses to acute stimulation. To determine the contribution of food restriction to the effects of osmotic stimulation, the function of the hypothalamic pituitary adrenal axis was analyzed in rats subjected to food deprivation, water deprivation or their combination for 60 h. In all three groups, basal levels of plasma corticosterone were increased, while ACTH and catecholamines were unchanged. Basal plasma vasopressin levels were normal in food deprived rats, but significantly increased in water deprived and simultaneously food and water deprived rats. In contrast to the 25% reduction of plasma ACTH responses to 30 min immobilization by water deprivation, food deprivation had no inhibitory effect and prevented the decreased ACTH responsiveness caused by water deprivation. In control rats, plasma corticosterone levels increased 22.5-fold 30 min after immobilization, and this response was significantly potentiated in the water deprived, food deprived and combined food and water deprived groups. The elevation in plasma catecholamines in response to acute immobilization was also enhanced in both water deprived and food deprived rats. In situ hybridization studies showed a 35% increase in VP mRNA levels in the PVN after water deprivation, whereas food deprivation caused a slight decrease and prevented the stimulatory effect of water deprivation. CRH mRNA in the PVN was reduced by 27% after food deprivation and by 67% after water deprivation, but simultaneous food and water deprivation caused a significantly smaller reduction similar to that in food deprivation alone.(ABSTRACT TRUNCATED AT 250 WORDS)
先前的研究表明,慢性缺水或摄入高渗盐水,这些伴随食物摄入量减少的渗透压应激模型,会降低下丘脑促肾上腺皮质激素释放激素(CRH)mRNA水平以及促肾上腺皮质激素(ACTH)对急性刺激的反应。为了确定食物限制对渗透压刺激效应的作用,对禁食、禁水或两者结合60小时的大鼠的下丘脑 - 垂体 - 肾上腺轴功能进行了分析。在所有三组中,血浆皮质酮的基础水平升高,而促肾上腺皮质激素和儿茶酚胺未发生变化。禁食大鼠的基础血浆血管加压素水平正常,但禁水以及同时禁食禁水的大鼠中该水平显著升高。与禁水导致血浆促肾上腺皮质激素对30分钟固定应激的反应降低25%相反,禁食没有抑制作用,并且阻止了由禁水引起的促肾上腺皮质激素反应性降低。在对照大鼠中,固定应激30分钟后血浆皮质酮水平增加了22.5倍,并且在禁水、禁食以及禁食禁水联合组中该反应显著增强。在禁水和禁食的大鼠中,急性固定应激引起的血浆儿茶酚胺升高也增强。原位杂交研究表明,禁水后室旁核(PVN)中血管加压素mRNA水平增加35%,而禁食导致轻微下降并阻止了禁水的刺激作用。禁食后室旁核中的促肾上腺皮质激素释放激素mRNA减少27%,禁水后减少67%,但同时禁食禁水导致的减少明显较小,类似于单独禁食的情况。(摘要截断于250字)