Artery Research

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Volume 20, Issue C, December 2017, Pages 83 - 84

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

Authors
Frederic Roca1, 2, 3, 4, Jeremy Bellien1, 2, 3, 4, Michele Iacob1, 2, Robinson Joannides1, 2, 5, 4
1Rouen University Hospital, Department of Pharmacology, F 76000 Rouen, France
2Normandie Univ, UNIROUEN, Inserm U1096, F 76000, Rouen, France
3University of Rouen, Institute for Research and Innovation in Biomedicine, Rouen, France
4Clinical Investigation Center CIC-CRB 1404, Rouen University Hospital, Rouen, France
5University of Rouen, Institute for Research and Innovation in Biomedicine, Rouen, France
Available Online 6 December 2017.
DOI
10.1016/j.artres.2017.10.117How to use a DOI?
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.

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This is an open access article distributed under the CC BY-NC license.

References

1.F Roca, J Bellien, M Iacob, I Remy-Jouet, and R Joannides, Evidence for a role of vascular endothelium in the control of arterial wall viscosity in humans, 2017. Submitted.
2.P Boutouyrie, Y Bézie, P Lacolley, P Challande, P Chamiot-Clerc, A Benetos, et al., In vivo/in vitro comparison of rat abdominal aorta wall viscosity. Influence of endothelial function, Arterioscler Thromb Vasc Biol, Vol. 17, No. 7, Jul 1997, pp. 1346-55.
3.J Bellien, M Iacob, I Remy-Jouet, D Lucas, C Monteil, L Gutierrez, et al., Epoxyeicosatrienoic acids contribute with altered nitric oxide and endothelin-1 pathways to conduit artery endothelial dysfunction in essential hypertension, Circulation, Vol. 125, No. 10, 13 Mar 2012, pp. 1266-75.
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Journal
Artery Research
Volume-Issue
20 - C
Pages
83 - 84
Publication Date
2017/12/06
ISSN (Online)
1876-4401
ISSN (Print)
1872-9312
DOI
10.1016/j.artres.2017.10.117How to use a DOI?
Open Access
This is an open access article distributed under the CC BY-NC license.

Cite this article

risenwbib
TY  - JOUR
AU  - Frederic Roca
AU  - Jeremy Bellien
AU  - Michele Iacob
AU  - Robinson Joannides
PY  - 2017
DA  - 2017/12/06
TI  - P168 ENDOTHELIAL REGULATION OF AWV IS IMPAIRED DURING INCREASE IN BLOOD FLOW IN ESSENTIAL HYPERTENSION
JO  - Artery Research
SP  - 83
EP  - 84
VL  - 20
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2017.10.117
DO  - 10.1016/j.artres.2017.10.117
ID  - Roca2017
ER  -