P10: Loss of Endothelium-Dependent Regulation of Arterial Wall Viscosity in Essential Hypertension

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.