Artery Research

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Volume 20, Issue C, December 2017, Pages 64 - 64

P10 LOSS OF ENDOTHELIUM-DEPENDENT REGULATION OF ARTERIAL WALL VISCOSITY IN ESSENTIAL HYPERTENSION

Authors
Frederic Roca1, 2, 3, 4, Jeremy Bellien1, 2, 3, 4, Michele Lacob1, 2, 3, 4, Robinson Joannides1, 2, 3, 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
Available Online 6 December 2017.
DOI
10.1016/j.artres.2017.10.063How to use a DOI?
Abstract

Background: Nitric oxide (NO) and epoxyeicosatrienoic acids (EETs) regulate arterial wall viscosity (AWV) in young subjects (1). During hypertension, characterised by a decrease in endothelium-derived NO and an early disappearance of EETs, AWV is not modified (2,3). We compared the role of NO and EETs in the regulation of AWV in 18 middle-age untreated hypertensive patients (HT) vs. 14 matched normotensive controls (NT).

Methods: Radial artery diameter and pressure were measured before and after infusion of L-NMMA, fluconazole or both. 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, bounded by pulse pressure and diameter (WE, elastic energy stored).

Results: At baseline, WV and WE were higher in HT than in NT (WV: 0.71 [0.65–1.19] vs. 0.45 [0.40–0.62] mmHg.mm2, p < 0.05; WE: 1.99 [1.45–2.61] vs. 1.09 [0.96–1.54] mmHg.mm2, p < 0.01) but WV/WE were similar (40.3 ± 7.1% vs. 40.5 ± 5.9%). In NT, fluconazole and L-NMMA decreased diameter, but did not modify WV, WE and WV/WE. L-NMMA + fluconazole decreased diameter and increased WV/WE (38.9 ± 8.5% to 47.5 ± 8.9%, p < 0.05) due to an increase in WV (+27.1 ± 57.5%) as compared to WE (−1.3±27.8%) (p < 0.05). In HT, whereas fluconazole had no effect on diameter, WV and WE, LNMMA and LNMMA + fluconazole decreased these parameters (p < 0.05) without change in WV/WE.

Conclusion: In NT, NO and EETs regulate AWV of conduit arteries. Conversely, in HT associated to an increased elastic energy stored, NO regulates elastic work but not AWV that remains stable. Whether this represents an optimal adaptation remains to be investigated.

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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.RL Armentano, JG Barra, DB Santana, FM Pessana, S Graf, D Craiem, et al., Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition, Hypertension, Vol. 47, No. 3, Mar 2006, pp. 384-90.
3.F Roca, M Iacob, G Feugray, C Thuillez, J Bellien, and R Joannides, Impaired regulation of arterial wall viscosity during changes in blood flow in essential hypertensive patients, Artery Research, Vol. 16, 1 Dec 2016, pp. 77-8.
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Journal
Artery Research
Volume-Issue
20 - C
Pages
64 - 64
Publication Date
2017/12/06
ISSN (Online)
1876-4401
ISSN (Print)
1872-9312
DOI
10.1016/j.artres.2017.10.063How 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 Lacob
AU  - Robinson Joannides
PY  - 2017
DA  - 2017/12/06
TI  - P10 LOSS OF ENDOTHELIUM-DEPENDENT REGULATION OF ARTERIAL WALL VISCOSITY IN ESSENTIAL HYPERTENSION
JO  - Artery Research
SP  - 64
EP  - 64
VL  - 20
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2017.10.063
DO  - 10.1016/j.artres.2017.10.063
ID  - Roca2017
ER  -