Endothelium-dependent adaptation of arterial wall viscosity during blood flow increase is impaired in essential hypertension.

BACKGROUND AND AIMS

Arterial wall viscosity (AWV) is regulated by endothelium-derived NO and epoxyeicosatrienoic acids (EETs) under baseline physiological conditions. Whether these factors regulate AWV during blood flow increase and whether this mechanism is affected in essential hypertensive patients (HT) remain unknown.

METHODS

The evolution of radial artery diameter, wall thickness and arterial pressure in response to an increase in flow induced by hand skin heating were measured in 18 untreated HT and 14 normotensive controls (NT) during local infusion of saline and the respective pharmacological inhibitors of NO-synthase and EETs synthesis by cytochrome P450, L-NMMA and/or fluconazole. AWV was estimated by the ratio of the viscous energy dissipated (W) to the elastic energy stored (W) obtained from the pressure-diameter relationship. Concomitant changes in operating conditions, which influence the AWV, were taken into account by calculating the midwall stress.

RESULTS

Baseline W and W were higher in HT than in NT but W/W was similar. In saline condition, W/W increased in HT during heating but not in NT. In the presence of L-NMMA and/or fluconazole, W/W increased during heating in NT. In contrast, these inhibitors did not modify the increase in W/W during heating in HT compared to saline. In all conditions, a larger increase in W than W was responsible for the increase in W/W.

CONCLUSIONS

The release of NO and EETs maintains a stable AWV 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.