Mechanisms and Clinical Implications of Endothelial Dysfunction in Arterial Hypertension

Abstract

The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities.

Restoration of Mitochondrial Function Is Essential in the Endothelium-Dependent Vasodilation Induced by Acacetin in Hypertensive Rats

“…Endothelial dysfunction is not a specific feature of hypertension, but it is common to the majority of cardiovascular risk factors [ 1 ]. In particular, patients with hypertension presented greater apoptosis in the endothelium [ 34 , 40 ]. In line with recent reports, cell apoptosis investigated by Annexin V–FITC/PI flow cytometry assay and Hoechst 33342/PI double staining revealed that the percentage of apoptotic cells induced by Ang II was notably reduced by acacetin.…”

Endothelial Dysfunction, Oxidative Stress and Inflammation: Implications in Atherogenesis, Cardiovascular Diseases and Gene Targeted Therapeutic Approach

“…2). In addition, ECs are also involved in smooth muscle cells proliferation and migration via balanced vasoconstriction and vasodilation as well as platelets aggregation and adhesion 2,32 and thrombogenesis. Thus, unsettling this tightly regulated equilibrium leads to endothelial dysfunction.…”

Effects of physical exercise associated with a diet enriched with natural antioxidants on cerebral hypoperfusion and reperfusion injury in spontaneously hypertensive rats

“…It has been reported that about 87% of transient ischemic attacks/minor strokes (TIAs/MSs) are caused by narrowed or obstructed blood vessels in the brain cutting off the blood flow to neurons ( Ganzer et al, 2016 ; Yu and Coutts 2018 ; Panuganti et al, 2022 ). Several studies demonstrate that the pathogenesis of hypertension is associated with oxidative stress, with a reduction in the bioavailability of nitric oxide (NO) accompanied by endothelial dysfunction and alterations in the structure of cerebral blood vessels, disrupting complex vasoregulatory mechanisms ( Atochin and Huang 2011 ; Zhu et al, 2016 ; Quick et al, 2021 ; Ambrosino et al, 2022 ).…”