Heat shock protein 90 is involved in pulsatile flow-induced dilation of rat middle cerebral artery

The physical forces exerted on the blood vessel walls by the passage of intravascular blood are pressure and shear stress. These are derived from the movement of blood by the action of the heart. Fluid shear stress and circumferential stretch play important roles in maintaining homeostasis of the blood vessel [1]. Since active vascular resistance in vivo is determined primarily by the tone of small arteries [2], it is important to study cellular responses of cells in the wall of such arteries to hemodynamic factors. Pulsatile flow in isolated cerebral arteries from piglets has been found to induce dilation which was dependent on the activity of nitric oxide synthase (NOS) [3], However, whether dilation of the artery by pulsatile flow is unique to neonatal cerebral arteries and the mechanism by which an acute change in pulsatility causes activation of NOS is not clear. A recent study by Garcia-Cardena et al, [4] suggested that acute activation of endothelial NOS (eNOS) is mediated by one of the heat shock proteins, Hsp90, which is known to coordinate the trafficking and regulation of diverse proteins [5]. In the present study, we demonstrate that in isolated middle cerebral arteries from adult rats, pulsatile flow induces NOS-dependent dilation, and that Hsp90 is involved in the pulsatile flow-induced dilation.