P168 ENDOTHELIAL REGULATION OF AWV IS IMPAIRED DURING INCREASE IN BLOOD FLOW IN ESSENTIAL HYPERTENSION

Abstract

Background: Arterial wall viscosity (AWV) depends on endothelium-derived factors in physiological conditions (1,2). Hypertension is characterized by an altered FMD during sustained flow increase due to endothelial dysfunction (3). Whether NO and EETs regulate change in AWV during increase in flow in hypertensive patients (HT) as compared with normotensive controls (NT) remains to be evaluated. Methods: Radial artery diameter, wall thickness and arterial pressure were measured in 18 untreated essential HT and 14 frequency matched NT during hand skin heating with saline, L-NMMA, fluconazole, or both inhibitors infusion. AWV was estimated by the ratio of the area of the hysteresis loop of the pressure-diameter relationship (WV, viscous energy dissipated) to the area under the loading phase (WE, elastic energy stored). Results: During saline infusion, WV, WE and WV/WE were not modified after heating in NT whereas WV/WE increased in HT (39.3±12.0% to 49.9±7.7%, p < 0.05) due to a larger increase in WV than WE (ΔWV: +41.5±27.6% vs. ΔWE: +25.1±28.4%, p < 0.05). With all inhibition sequences, WV/WE increased after heating in NT (p < 0.05) due to a larger increase in WV than WE (p < 0.05). In HT with fluconazole, L-NMMA and L-NMMA + fluconazole, WV/WE increased after heating (p < 0.05) due to a larger increase in WV than WE (p < 0.05), similarly to saline infusion. In all conditions, increase in shear stress was similar between NT and HT. Conclusion: NO and EETs maintain stable AWV during change in flow in NT, and this regulation is lost in HT resulting in an increased AWV after heating.