Moderate hypoxia increases heat shock protein 90 expression in excised rataorta

We hypothesized that heat shock protein 90 (HSP90) expression would be incr eased in vascular tissue exposed to a hypoxic stress th at resulted in alte red contractile function. We tested this hypothesis by subjecting excised r at aortic rings to a hypoxic stress that has been shown to reduce contracti le force induced by arginine vasopressin (PO2 approximate to 50 mm Hg for 1 h) and determining the effect on HSP90 expression. Concentration-response curves were determined for control and hypoxic excised rat aortic rings exp osed to norepinephrine (n = 8) or KCl (n = 8). Hypoxia reduced the force ge nerated in response to the highest concentration of each agonist. HSP90 exp ression was evaluated by immunoblotting (n = 6) and immunohistochemistry (n = 7) Both methods documented increased expression of HSP90 in hypoxic aort ae as compared to controls. HSP90 expression was increased within the cytop lasm and in conjunction with the nucleus of vascular smooth muscle cells in the tunica media and also within vascular myointimal cells. We conclude th at a hypoxic stress sufficient to induce contractile dysfunction increases HSP90 expression in rat aortic smooth muscle cells. Copyright (C) 1999 S. K arger AG. Basel.