We previously demonstrated that restraint and pharmacological agents t
hat activate sympathetic nervous system activity induce expression of
the 70-kD heat shock protein (HSP70) in major blood vessels. The magni
tude and rapidity in which HSP70 is induced in the aorta suggest that
it may play a salient role in the mechanical properties of vascular sm
ooth muscle. Other investigators have reported that HSP70 inducibility
is increased in genetically hypertensive animals. In this report, we
have investigated the effects of acute and chronic (8-week) exposure t
o restraint and restraint in the presence of a randomized intermittent
air jet on the development of hypertension and the induction of HSP70
in the aorta and adrenal glands of normotensive adult male Sprague-Da
wley rats. Acute restraint or air jet resulted in a fivefold to sixfol
d increase in aortic HSP70 mRNA expression. Chronic exposure to restra
int reduced the HSP70 response to acute restraint. In contrast, no ada
ptation of the HSP70 response to acute air jet was observed in aortas
of chronically air jet-treated rats. In adrenal glands, HSP70 expressi
on was reduced after chronic restraint and air jet, indicating that in
this tissue, adaptation occurs to both stressors. There was no differ
ence in HSP70 expression in unstressed rats that had been chronically
exposed to restraint or air jet in either adrenal gland or aorta. A si
gnificant increase (P<.05) in systolic blood pressure developed in air
jet-treated animals (120+/-3 mm Hg) but not in restrained rats (107+/
-2 mm Hg) compared with unstressed controls (106+/-3 mm Hg). Plasma ca
techolamine concentrations were not indicative of HSP70 expression in
the aorta. From these results, we conclude that adaptation to a stress
or influences both resting blood pressure and the magnitude of the HSP
70 response in aorta to an acute stress. Thus, the ability to induce H
SP70 in vascular tissue may contribute to the development of hypertens
ion in chronically stressed animals.