<p>Thrombospondin-1 Serum Levels In Hypertensive Patients With Endothelial Dysfunction After One Year Of Treatment With Perindopril</p>

Abstract

BackgroundThrombospondin-1 (TSP-1) is a matricellular functional protein of the extracellular matrix. As it is not constitutively present extracellularly, its secretion is enhanced in several situations, namely injury, chronic pathology, tissue remodeling, angiogenesis, and aging. Over the last decade, TSP-1 has been reported to be involved in complex and opposing biological effects on vasculature in the context of NO signaling. Several studies have reported high patient TSP-1 plasma levels, indicating that the protein can potentially serve as a prognostic marker for pulmonary arterial hypertension.Materials and methodsHere, we aimed to quantify TSP-1 serum levels in hypertensive patients with endothelial dysfunction before and after one year of treatment with Perindopril (an antihypertensive drug with vasoprotective properties).ResultsAfter one year of treatment, TSP-1 levels increased in hypertensive patients compared to baseline (T0: 8061.9 ± 3684.80 vs T1: 15380±5887 ng/mL, p<0.001) and compared to non-hypertensive controls (9221.03 ± 6510.21 ng/mL). In contrast, pentraxin-3 plasma levels were decreased after one year of Perindopril treatment in both hypertensive (T0: 0.91 ± 0.51 vs T1: 0.50 ± 0.24 ng/mL, p<0.001) and control group (1.36 ±1.5 ng/mL) patients, although flow-mediated vasodilation and intima-media thickness assessment parameters were not significantly changed. Systolic and diastolic blood pressure values as well as levels of fibrinogen, high-sensitivity C-reactive protein, triglycerides, and alanine aminotransferase were found to be significantly lower after one year of treatment with Perindopril. High levels of TSP-1 strongly correlated with platelet count (positive), lymphocytes (positive), red cell distribution width-CV (positive), systolic blood pressure (negative), and mean corpuscular hemoglobin (negative) after one year of treatment. Blood urea nitrogen was found to be a protective factor for TSP-1, while glucose and heart rate were found to be risk factors prior to and after treatment.

Vascular Extracellular Matrix Remodeling and Hypertension

“…Notably, some ECM alterations are specific to certain treatments. For instance, serum TSP-1 levels in hypertensive patients are upregulated by treatment with perindopril (ACEI) but not other kinds of antihypertensive drugs, suggesting that TSP-1 could be a specific biomarker for ACEI efficacy (18,19). Several nonclassical therapeutic strategies have also been used in preclinical studies.…”

Cardioprotective Effects of Cultivated Black Chokeberries (Aroniaspp.): Traditional Uses, Phytochemistry and Therapeutic Effects

“…Thus, it plays an essential role in the pathogenesis of several cardiovascular (hypertension, atherosclerosis, systemic and pulmonary hypertension, etc. ), as well as other diseases (inflammatory diseases or cancer) (Figure 2) [60][61][62].…”

“…Apart from endothelial dysfunction, it will induce smooth muscle cell migration, vascular calcification, oxidative stress, degradation of extracellular matrix and collagen, elastolysis and increased activity of metalloproteinases. Vascular inflammation was observed in patients with hypertension, metabolic syndrome, diabetes, infections, preeclampsia, coronary heart disease or peripheral arterial disease [58,62]. Thus, the anti-inflammatory effect exhibited by several bioactive natural, synthetic or semi-synthetic compounds is important for the prevention of chronic diseases (especially the cardiovascular, metabolic and immune system disorders) and also for decreasing their complications [16].…”

Cardiovascular Risk Factors for Different Types of Psychiatric Pathologies. A Correlative Study

“…There are also established studies that have elucidated similar mechanisms regarding the etiopathogenesis of Alzheimer's disease and atherosclerotic disease [37], such as a common genetic and behavioural background [42]. Hypertension is identified as an independent factor for Alzheimer's disease [5][6][7]10]. There are theories about the etiopathogenesis of Alzheimer's disease related to vascular wall thickening and blood vessel occlusion, a pathology that is generated by atherosclerosis [43].…”