Effects of Aspirin on Endothelial Function and Hypertension

Mikhail S Dzeshka, Alena Shantsila, Gregory Y H Lip, Mikhail S Dzeshka, Alena Shantsila, Gregory Y H Lip

Abstract

Purpose of review: Endothelial dysfunction is intimately related to the development of various cardiovascular diseases, including hypertension, and is often used as a target for pharmacological treatment. The scope of this review is to assess effects of aspirin on endothelial function and their clinical implication in arterial hypertension.

Recent findings: Emerging data indicate the role of platelets in the development of vascular inflammation due to the release of proinflammatory mediators, for example, triggered largely by thromboxane. Vascular inflammation further promotes oxidative stress, diminished synthesis of vasodilators, proaggregatory and procoagulant state. These changes translate into vasoconstriction, impaired circulation and thrombotic complications. Aspirin inhibits thromboxane synthesis, abolishes platelets activation and acetylates enzymes switching them to the synthesis of anti-inflammatory substances. Aspirin pleiotropic effects have not been fully elucidated yet. In secondary prevention studies, the decrease in cardiovascular events with aspirin outweighs bleeding risks, but this is not the case in primary prevention settings. Ongoing trials will provide more evidence on whether to expand the use of aspirin or stay within current recommendations.

Keywords: Arterial hypertension; Aspirin; Cyclooxygenase; Endothelial function; Inflammation; Platelets.

Conflict of interest statement

Drs. Dzeshka, Shantsila, and Lip declare no conflicts of interest relevant to this manuscript. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors.

Figures

Fig. 1
Fig. 1
Influence of aspirin on endothelial function. * Various receptors participate in cellular interactions. 15R-HETE, 15-Hydroxyeicosatetraenoic acid; 5-HT, serotonin; 5-LOX, 5-lipooxygenase; AA, arachidonic acid; AC, adenylate cyclase; IP, prostacyclin receptor; ADP, adenosine diphosphate; ALX, ATL receptor; ASA, acetyl salicylic acid; Ac, acetyl group; ATL, aspirin-triggered 15-epi-lipoxin A4; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; cGMP, cyclic guanosine monophosphate; COX, cyclooxygenase; CXCL1, 4, 5, 7, 8, 12, chemokine (C-X-C motif) ligand 1, 4, 5, 7, 8 and 12, respectively; EDHF, endothelium-derived hyperpolarising factor; EGF, epidermal growth factor; eNOS, endothelial nitric oxide synthase; FV, XI, XIII, coagulation factors V, XI, XIII, respectively; FGF, fibroblast growth factor; GPVI, collagen receptor; GTP, guanosine triphosphate; HO-1, heme oxygenase 1; IGF, insulin-like growth factor; IL-1β, interleukin-1β; IL-6, interleukin-6; MCP-1, monocyte chemoattractant protein 1; MIP-1α, macrophage inflammatory protein 1α; MMP-1, 2, 9, matrix metalloproteinase 1, 2 and 9, respectively; mRNA, matrix ribonucleic acid; NO, nitric oxide; NOX, nicotinamide adenine dinucleotide phosphate-oxidase; PDGF, platelet-derived growth factor; PgG2/H2, prostaglandin G2/H2; PgI2, prostacyclin; PGIS, prostacyclin synthase; PSGL-1, P-selectin glycoprotein ligand 1; RANTES, regulated on activation, normal T Cell expressed and secreted; S1P, phingosine-1-phosphate; S1P2, S1P receptor 2; sGC, soluble guanylate cyclase; SMC, smooth muscle cell; TGF-β1, transforming growth factor beta 1; TIMP-1, 4, tissue inhibitor of MMP 1 and 4, respectively; TNF-α, tumour necrosis factor α; TP, thromboxane prostanoid receptor; TSP-1, thrombospondin 1; TxA2, thromboxane A2; TXAS, thromboxane A2 synthase; VEGF, vascular endothelial growth factor; vWF, von Willebrand factor

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