ACUTE HYPERTENSION INDUCES HEAT-SHOCK PROTEIN-70 GENE-EXPRESSION IN RAT AORTA

Background Many factors cause acute systemic hypertension, which in tu rn can result in damage to the vessel wall and lead to vascular diseas e. In previous studies, we demonstrated that restraint, or immobilizat ion stress, results in the induction of heat-shock protein 70 (hsp70) gene expression in the aorta of adult rat and showed that this respons e was markedly attenuated with age. Methods and Results Here we provid e evidence that restraint-induced hsp70 expression occurs secondary to a rise in systemic blood pressure. Old rats were unable to mount a si gnificant stress-induced hypertensive response, providing an explanati on for the reduced hsp70 response in the old rats. A variety of vasoac tive agents that induce acute hypertension through distinct signal tra nsduction pathways, including phenylephrine, dopamine, vasopressin, an giotensin II, and endothelin-1, were found to result in hsp70 mRNA ind uction in the aorta. The magnitude of hsp70 expression achieved with t hese hypertensive agents was directly correlated with their relative e ffects on blood pressure. Rats were treated with the vasodilator sodiu m nitroprusside, which prevented an acute rise in blood pressure from the hypertensive agents tested and abolished induction of hsp70 expres sion. Conclusions These findings support the conclusion that hsp70 ind uction occurs as a physiological response to acute hypertension and su ggest the possibility that hsp70 plays a role in the protecting the va sculature from damage during hemodynamic stress.