Joseph L. Unthank
To my knowledge, you and Dr. Wang were the first to demonstrate that shear stress is elevated after hypertension is established. You comment in your presentation that "The arterial remodeling during the development of hypertension is not pathological but merely an adaptation to the mechanical forces imposed on the vessels in the face of their main goal to autoregulate blood flow." While this hypothesis is attractive, if the structural changes within the wall depend upon endothelial dysfunction as you suggest, I wonder if it is not pathological. If it were purely physiologic, it would seem that medial thickening could occur to reduce circumferential wall stress while maintaining normal shear stress. The increase in shear stress suggests that either the set point for regulation of shear stress is elevated in hypertension or the ability of the vessels to respond to shear is suppressed. Data summarized by Tuttle in this symposium with our "collateral" model suggests that the latter is the case. Thus, it appears to me that while the adaptations to hypertension may not initially be "pathological", by the time endothelial dysfunction occurs and the vessels are not able to properly respond to shear the response is pathological. What do you think?