Vascular expression of heat shock protein 72 in fructose-induced hypertensive rats

Heat shock proteins (HSPs) have been implicated in protecting the cardiovascular system and in the pathogenesis of hypertension in stressed animals. In the present study, we used a fructose-induced hypertension model to explore the vascular expression of HSP72, the major inducible heat shock protein, in response to stress. Normal Sprague-Dawley rats gradually developed hypertension about 2 weeks after feeding with fructose-enriched diet and the elevated blood pressure became stable 5 weeks following diet treatment. The in vivo expression of HSP72 was absent in control rats but was transiently induced in the aorta of fructose-fed rats during the development of hypertension. Aortic HSP72 was undetectable at the established phase of hypertension. The expression of HSP72 in responses to heat shock, or vasoactive agents were examined in cultured aortic smooth muscle cells. Heat shock induced the expression of HSP72 in cells from fructose-fed rats and age-matched control rats, and the expression levels were generally not significantly varied at different sampling time points in either cell source. Also, there was no apparent difference in the magnitude of HSP72 expression between two cell sources at each selected time point. Norepinephrine or angiotensin II induced a similar level of HSP72 expression in either cell source regardless of sampling time point. These data suggest that HSP72 is associated with the development of hypertension in this model and may exert protective effect on the vasculature in response to hemodynamic stress during the early stage of hypertension.