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Pathophysiology of hypertension: interactions between macro and microvascular alterations through endothelial dysfunction

Yannoutsos, Alexandraa; Levy, Bernard I.b; Safar, Michel E.a; Slama, Gerarda; Blacher, Jacquesa

doi: 10.1097/HJH.0000000000000021

Hypertension is a multifactorial systemic chronic disorder through functional and structural macrovascular and microvascular alterations. Macrovascular alterations are featured by arterial stiffening, disturbed wave reflection and altered central to peripheral pulse pressure amplification. Microvascular alterations, including altered wall-to-lumen ratio of larger arterioles, vasomotor tone abnormalities and network rarefaction, lead to disturbed tissue perfusion and susceptibility to ischemia. Central arterial stiffness and microvascular alterations are common denominators of organ damages. Vascular alterations are intercorrelated, amplifying the haemodynamic load and causing further damage in the arterial network. A plausible precursor role of vascular alterations in incident hypertension provides new insights for preventive and therapeutic strategies targeting macro and microvasculature. Cumulative metabolic burden and oxidative stress lead to chronic endothelial injury, promoting structural and functional vascular alterations, especially in the microvascular network. Pathophysiology of hypertension may then be revisited, based on both macrovascular and microvascular alterations, with a precursor role of endothelial dysfunction for the latter.

aDiagnosis and Therapeutics Centre, Hypertension and Cardiovascular Prevention Unit, Hôtel-Dieu Hospital

bPARCC, INSERM U970, and Blood and Vessels Institute, Lariboisière Hospital, Paris, France

Correspondence to Jacques Blacher, Université Paris Descartes, Faculté de Médecine, Assistance Publique-Hôpitaux de Paris, Unité HTA, Prévention et Thérapeutique Cardiovasculaires, Centre de Diagnostic et de Thérapeutique, Hôtel-Dieu, Place du Parvis Notre-Dame, 75004 Paris, France. Tel: +33 0 1 42 34 89 66; fax: +33 0 1 42 34 86 32; e-mail:

Abbreviations: AGE, advanced glycation end-products; TGF-β, transforming growth factor-beta

Received 23 May, 2013

Accepted 10 September, 2013

© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins