Arterial wall viscosity is regulated by endothelium-derived NO and epoxyeicosatrienoic acids (EETs) under baseline physiological conditions. Whether these factors regulate arterial viscosity during blood flow increase and whether this mechanism is affected in patients with essential hypertensive have remained unknown.
In a recent publication in Atherosclerosis Dr Roca et al showed in a study of 18 untreated hypertensive patients and 14 normotensive controls that baseline arterial viscosity was increased in hypertensive patients. Whereas pharmacological inhibition of NO and/or EETs increased arterial viscosity in response to flow-mediated dilatation, these inhibitors did not modify the arterial viscosity in hypertensive patients.
Thus, the release of NO and EETs maintains a stable arterial wall viscosity during flow increase and this endothelial adaptive regulation is lost during essential hypertension, which may promote excessive viscous energy dissipation and cardiovascular uncoupling. Restoration of EETs availability with inhibitors of soluble epoxide hydrolase could thus constitute a promising pharmacological approach to restore the endothelial adaptive regulation of AWV.
Our publication demonstrating the benefits of PTP1B gene deletion on the cardiovascular consequences of aging published in Am J Physiol PMID: 29569957