Blood Pressure and Heat Shock Protein Expression in Response to Acute and Chronic Stress

Abstract

Abstract We previously demonstrated that restraint and pharmacological agents that activate sympathetic nervous system activity induce expression of the 70-kD heat shock protein (HSP70) in major blood vessels. The magnitude and rapidity in which HSP70 is induced in the aorta suggest that it may play a salient role in the mechanical properties of vascular smooth 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 to 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-Dawley rats. Acute restraint or air jet resulted in a fivefold to sixfold increase in aortic HSP70 mRNA expression. Chronic exposure to restraint reduced the HSP70 response to acute restraint. In contrast, no adaptation of the HSP70 response to acute air jet was observed in aortas of chronically air jet–treated rats. In adrenal glands, HSP70 expression was reduced after chronic restraint and air jet, indicating that in this tissue, adaptation occurs to both stressors. There was no difference in HSP70 expression in unstressed rats that had been chronically exposed to restraint or air jet in either adrenal gland or aorta. A significant 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 catecholamine concentrations were not indicative of HSP70 expression in the aorta. From these results, we conclude that adaptation to a stressor influences both resting blood pressure and the magnitude of the HSP70 response in aorta to an acute stress. Thus, the ability to induce HSP70 in vascular tissue may contribute to the development of hypertension in chronically stressed animals.