Activity of the hypothalamic pituitary adrenal axis and sympathoadrenal system during food and water deprivation in the rat.
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)
Kiss
A
A
Developmental Endocrinology Branch, National Institute of, Child Health and Human Development, NIH, Bethesda, MD 20892.
Jezova
D
D
Aguilera
G
G
D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005508:Food Deprivation; D015870:Gene Expression; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D007031:Hypothalamus / Q000378:metabolism; D017403:In Situ Hybridization; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010121:Oxytocin / Q000096:biosynthesis; D010913:Pituitary-Adrenal System / Q000502:physiology*; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis; D011388:Prolactin / Q000097:blood; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018019:Receptors, Corticotropin-Releasing Hormone / Q000378:metabolism; D017483:Receptors, Vasopressin / Q000378:metabolism; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000503:physiopathology*; D014667:Vasopressins / Q000096:biosynthesis / Q000097:blood; D014868:Water Deprivation
D012333:RNA, Messenger; D018019:Receptors, Corticotropin-Releasing Hormone; D017483:Receptors, Vasopressin; D014667:Vasopressins; D010121:Oxytocin; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D003346:Corticotropin-Releasing Hormone; D004298:Dopamine; D003345:Corticosterone; D009638:Norepinephrine; D004837:Epinephrine