Format

Send to

Choose Destination
Atherosclerosis. 2019 Jun;285:102-107. doi: 10.1016/j.atherosclerosis.2019.04.208. Epub 2019 Apr 8.

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

Author information

1
Rouen University Hospital, Department of Pharmacology, F 76000, Rouen, France; Normandie Univ, UNIROUEN, Inserm U1096, F 76000, Rouen, France; University of Rouen, Institute for Research and Innovation in Biomedicine, Rouen, France; Clinical Investigation Center CIC-CRB 1404, Rouen University Hospital, Rouen, France. Electronic address: frederic.roca@chu-rouen.fr.
2
Rouen University Hospital, Department of Pharmacology, F 76000, Rouen, France; Normandie Univ, UNIROUEN, Inserm U1096, F 76000, Rouen, France; University of Rouen, Institute for Research and Innovation in Biomedicine, Rouen, France; Clinical Investigation Center CIC-CRB 1404, Rouen University Hospital, Rouen, France.
3
Rouen University Hospital, Department of Pharmacology, F 76000, Rouen, France; Normandie Univ, UNIROUEN, Inserm U1096, F 76000, Rouen, France.

Abstract

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

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.

KEYWORDS:

Arterial wall viscosity; Endothelial dysfunction; Endothelium; Epoxyeicosatrienoic acids; Hypertension; Nitric oxide

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center