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Pulsatile Stress, Arterial Stiffness, and Endothelial Function

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Abstract

Vascular endothelium contributes in humans to the regulation of conduit artery mechanical properties at baseline and during the increase in flow. This effect results from the shear stress-dependent release of vasoactive factors, as nitric oxide (NO) and endothelium-derived hyperpolarizing factors as epoxyeicosatrienoic acids (EETs) to modify arterial tone, geometry, and trophicity and to optimize vascular functions and cardiovascular coupling. Endothelial dysfunction appears as a major determinant of arterial stiffening, increased pulse pressure, and systolic hypertension, and in turn strategies protecting the endothelium prevent these abnormalities. In addition, endothelium also integrates pulsatile stimuli (pulse pressure and flow) to increase NO and EET release under physiological conditions, and the reduced pulse pressure-dependent strain in stiff conduits may suppress this adaptive response, thus amplifying the stiffening process. This article details fundamental experiments and clinical studies supporting these mechanisms.

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Joannidès, R., Bellien, J., Thuillez, C. (2014). Pulsatile Stress, Arterial Stiffness, and Endothelial Function. In: Safar, M., O'Rourke, M., Frohlich, E. (eds) Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. Springer, London. https://doi.org/10.1007/978-1-4471-5198-2_10

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