Venous endothelial function in cardiovascular disease

Abstract

The essential role of the endothelium in vascular homeostasis is associated with the release of endothelium-dependent relaxing and contractile factors (EDRF and EDCF, respectively). Different from arteries, where these factors are widely studied, the vasoactive factors derived from the venous endothelium have been given less attention. There is evidence for a role of the nitric oxide (NO), endothelium-dependent hyperpolarization (EDH) mechanism, and cyclooxygenase (COX)-derived metabolites as EDRFs; while the EDCFs need to be better evaluated since no consensus has been reached about their identity in venous vessels. The imbalance between the synthesis, bioavailability, and/or action of EDRFs and/or EDCFs results in a pathological process known as endothelial dysfunction, which leads to reduced vasodilation and/or increased vasoconstriction. In the venous system, endothelial dysfunction is relevant since reduced venodilation may increase venous tone and decrease venous compliance, thus enhancing mean circulatory filling pressure, which maintains or modify cardiac workload contributing to the etiology of cardiovascular diseases. Interestingly, some alterations in venous function appear at the early stages (or even before) the establishment of these diseases. However, if the venous endothelium dysfunction is involved in these alterations is not yet fully understood and requires further studies. In this sense, this article aims to review the current knowledge on venous endothelial function and dysfunction, and the general state of the venous tone in two important cardiovascular diseases of high incidence and morbimortality worldwide: hypertension and heart failure.

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“…Changes in vein function may manifest early on, even before the onset of these diseases. However, is not yet fully understood if the venous endothelium dysfunction is involved in these alterations, so further studies are required [85]. This hypothesis may support our idea that berberine could be a more efficient phlebotonic than β-escin, because berberine generates vasorelaxation, avoiding endothelial damage and thus preventing the progression of VD.…”

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“…Furthermore, as previously mentioned, it possesses platelet inhibitor properties [21]. Consequently, a decrease in NO bioavailability usually occurs in tandem with a pro-thrombotic and pro-inflammatory cascade and a less flexible endothelial state [6,28,30].…”

“…The most well-defined EDRF is NO, which is the protector of the vascular wall, with anti-inflammatory and antioxidant properties [6,10,29,30]. In addition to being a potent vasodilator gatekeeping endothelial health, NO is also a concentration-dependent cell proliferation and apoptosis modulator, as low relative concentrations appear to promote cell proliferation and anti-apoptotic responses and vice-versa [12,31,32].…”

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“…During the functioning of the circulatory system, hemodynamic and biochemical events occur that ensure the optimized supply of oxygen and nutrients to peripheral tissues. Furthermore, the heart, as a central cardiac pump, triggers the systolic ejection of oxygen-rich blood into the arteries, leading to the perfusion of organs and tissues to maintain life, whether in physiological or altered conditions, such as during physical exercise, diabetes, and obesity [30][31][32][33]. Furthermore, hemodynamic homeostasis involves the precise regulation of blood pressure, coordinated by the autonomic nervous system and renal mechanisms, while blood composition is maintained by the processes of hematopoiesis and hormonal control [33][34][35][36].…”