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Mechanobiology of Arterial Hypertension

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Vascular Mechanobiology in Physiology and Disease

Part of the book series: Cardiac and Vascular Biology ((Abbreviated title: Card. vasc. biol.,volume 8))

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Abstract

Enhanced mechanical forces are imposed on small and large vessels in hypertension. The enhanced transmural pressure increases predominantly circumferential wall stress that is returned toward control by adaptive mechanisms such as active constriction and eutrophic remodeling with concomitant increases of wall thickness. However, other hemodynamic, mechanical stresses are enhanced by such adaptive responses. Specifically, wall shear stress rises by pressure-induced constriction in smaller vessels provoking an endothelium-dependent dilation. A fine balance between these two homeostatic mechanisms that control wall stress and wall shear stress determines vascular tone in small resistance vessels which is shifted in hypertension toward higher vascular tone with enhanced peripheral resistance. Wall shear stress equals the frictional pressure loss during blood flow and must be larger to keep downstream capillary pressure stable, in the face of an increased pressure head. In this light, adaptive responses that decrease luminal diameter to control wall stress appear as maladaptive and energy-consuming. In large arteries, wall thickening is also observed in hypertension. However, the main impact of hypertension in large arteries, specifically elastic proximal vessels, is the profound consequence on pulse wave transmission. Pressure distends elastic arteries and consequently changes their capacity to store further volume during cardiac ejection in systole. This capacity depends on distensibility or compliance (the inverse of stiffness) which is decreased solely due to higher pressure. Changes in stiffness attributable to structural changes in the vessel wall are only found in young hypertensive individuals. Nevertheless, pulse wave velocity is largely increased due to the less compliant arteries at the prevailing pressure. This impacts hemodynamics in the pulsatile compartment of the vascular system that is governed by the Moens–Korteweg equation and wave reflections with dramatic consequences on other organs in the long run.

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Acknowledgement

This work was supported by grants from the German Ministry of Research (BMBF) and the German Centre for Cardiovascular Research (DZHK).

Sources of Funding

Work in my lab is funded by grants from the German Ministry of Research (BMBF) and the German Centre for Cardiovascular Research (DZHK).

Conflict of Interest

The author declares that he has no conflict of interest.

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Authors and Affiliations

  1. Institut für Physiologie, Universität zu Lübeck, Lübeck, Germany

    Cor de Wit

  2. Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V. (German Center for Cardiovascular Research), Lübeck, Germany

    Cor de Wit

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Correspondence to Cor de Wit .

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Editors and Affiliations

  1. Department of Cardiovascular Physiology, Heidelberg University, Heidelberg, Germany

    Markus Hecker

  2. Experimental Cardiology Department of Cardiology, Thorax Center, Erasmus University Medical Center, Rotterdam, The Netherlands

    Dirk J. Duncker

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de Wit, C. (2021). Mechanobiology of Arterial Hypertension. In: Hecker, M., Duncker, D.J. (eds) Vascular Mechanobiology in Physiology and Disease. Cardiac and Vascular Biology, vol 8. Springer, Cham. https://doi.org/10.1007/978-3-030-63164-2_10

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