Recent reports indicate that Heat Shock Proteins (HSPs) are induced in
mammalian tissues as part of a homeostatic response to environmental
stressors. Administration of sympathomimetic drugs and neuroendocrine
stress hormones has been shown to evoke an HSP response in unstressed
animals indicating that cell signaling events exists that couple speci
fic neurotransmitter/hormone-receptor interactions with HSP expression
in mammalian tissues. Herein, we demonstrate that exposure of rats to
a cold ambient temperature (6 degrees C) results in increased express
ion of constitutive and inducible members of the HSP70 gene family in
association with increased expression of the mitochondrial uncoupling
protein in brown adipose tissue (BAT). Increased HSP70 expression was
not restricted to BAT because HSP70 was also induced in the aorta. Thi
s cord-induced HSP response is characterized by a transient increase i
n HSP70 protein and mRNA in both tissues during continued exposure. Ga
nglionic blockade prevented cold-induced HSP70 expression in BAT and a
orta, indicating that sympathetic activity is requisite to this respon
se. Administration of the alpha(1)-adrenergic receptor antagonist, pra
zosin, also blocked expression, further delineating possible signaling
mechanisms mediating this response. Apparently, cells in some mammali
an tissues have adopted unique cellular regulatory mechanisms to suppo
rt HSP induction that have been incorporated into the physiological re
sponse of the entire organism to an environmental stressor. Copyright
(C) 1996 Elsevier Science Inc.