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Endothelial dysfunction in systemic hypertension

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Endothelial Dysfunction and Inflammation

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Abstract

Hypertension, defined as a rise in arterial blood pressure in the absence of a specific cause, leads to a myriad of cardiovascular complications that account for a high number of deaths globally. Progress in understanding hypertension comes from pioneering studies of the vasculature in both in vivo and in vitro settings. A common factor in hypertension and cardiovascular diseases is a decrease in the bioavailability of nitric oxide (NO), a potent endogenous vasodilator and a direct marker of endothelial function. This phenomenon, called endothelial dysfunction (ED), has increasingly gained importance in cardiovascular pathogenesis. Indeed, clinical evidence supports strong associations between ED and cardiovascular disease arising from common risk factors such as smoking, diet, lack of exercise, aging and genetic determinants. Besides NO, other factors that are produced in the endothelium, such as prostacyclin and endothelium-derived hyperpolarizing factor, can also be involved with, or act synergistically in, ED. This chapter focuses on the importance of NO in settings of ED and hypertension, and discusses the arguments around ED as a cause or consequence of hypertension by providing experimental and clinical evidence. We also aim to highlight current therapeutic strategies to improve vascular health by targeting levels of NO synthesis and raise questions emphasizing the need to further our knowledge in the molecular determinants in ED and hypertension.

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Yu, C., Sharma, A., Trane, A., Bernatchez, P. (2010). Endothelial dysfunction in systemic hypertension. In: Dauphinee, S., Karsan, A. (eds) Endothelial Dysfunction and Inflammation. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0346-0168-9_6

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