Pentobarbital, but not Propofol, Suppresses Vasopressin-stimulated Heat Shock Protein 27 Induction in Aortic Smooth Muscle Cells

Abstract

Background Although it is known that systemic blood pressure decreases after the administration of pentobarbital or propofol, the mechanisms underlying the cardiovascular effects of these anesthetics are still poorly understood. The authors previously showed that vasopressin stimulates the induction of heat shock protein (HSP) 27, a low-molecular-weight HSP, by a protein kinase C-dependent manner in aortic smooth muscle A10 cells. It is recognized that HSP27 may act as a chaperone like high-molecular-weight HSPs such as HSP70. HSP27 is reportedly associated with agonist-induced contraction of vascular smooth muscle cells. The authors examined the effects of pentobarbital and propofol on the vasopressin-stimulated HSP27 induction in A10 cells. Methods Cultured A10 cells were pretreated with pentobarbital or propofol and then stimulated by vasopressin or 12-o-tetradecanoylphorbol 13-acetate (TPA). The effect of vasopressin on HSP70 was evaluated by Western blot analysis and compared with its effect on HSP27. The concentrations of HSP27 were determined by a specific immunoassay. The effect of pentobarbital on the expression levels of mRNA for HSP27 by vasopressin was evaluated by Northern blot analysis. Results Vasopressin induced HSP27 but had little effect on HSP70. At concentrations used clinically, pentobarbital inhibited the accumulation of HSP27 by vasopressin or TPA. Pentobarbital reduced the levels of mRNA for HSP27 induced by vasopressin. In contrast, propofol affected neither the vasopressin- nor TPA-induced HSP27 accumulation. Conclusions These results suggest that pentobarbital suppresses the vasopressin-stimulated HSP27 induction in vascular smooth muscle cells. This inhibitory effect is probably exerted at a point downstream from protein kinase C.