AJP - Endocrinology and Metabolism, Vol 241, Issue 6 420-E427, Copyright © 1981 by American Physiological Society
Hypothalamic control of endocrine thermogenesis
P. R. Marques, P. Illner, D. D. Williams, W. L. Gren, J. W. Kendall, S. L. Davis, D. G. Johnson and C. C. Gale
Hypothalamic and ruminal cooling raised serum thyrotropin (TSH),
adrenocorticotropin (ACTH), norepinephrine (NE), and glucose in conscious
goats in 20 degree C ambient temperature. Cooling of the preoptic anterior
hypothalamus (POAH) for 2 h initially evoked shivering and
vasoconstriction, leading to 1.5 degree C rise in rectal temperature (Tr).
Pituitary-thyroid activation by POAH cooling was shown by peak rises in TSH
of 60% at 40 min, in triiodothyronine (T3) of 54% at 80 min, and in
thyroxine (T4) of 40% at 140 min. At 60 min, ACTH and NE peaked at 57 and
65%, respectively. TSH, ACTH, and NE declined during the 2nd h of POAH
cooling as Tr plateaued; when POAH cooling was stopped, these hormones fell
below basal level as vasodilation and panting restored Tr to normal. In
contrast to the core hyperthermia evoked by POAH cooling, ruminal
intubation with O degree C water (1 liter/10 kg) led to general
hypothermia, Tpoah and Tr falling 1.6 degree C at 40 min. Pituitary-thyroid
responses were less but ACTH and NE more, compared with POAH cooling. TSH
peaked at 37% at 20 min, T3 at 55% at 60 min, and T4 at 18% at 200 min.
ACTH peaked at 250% at 30 min and NE at 120% at 20 min. Thermosensitive
neurons in the POAH seem to mediate more sensitive and complete control
over TSH than over ACTH, or NE release, whereas extrahypothalamic core
thermosensitivity (e.g., brain stem, spinal cord, abdomen) may influence
ACTH and NE more than TSH release.
