Abstract
Background: Low bioavailability of nitric oxide (NO) is related to the pathophysiology of preeclampsia (PE). In the present study, we investigated the effect of nebivolol (NEB), a β3-receptor agonist with vasodilator properties, on the NO synthesis in endothelial cells incubated with plasma from preeclamptic patients. Methods and results: Human umbilical vein endothelial cells (HUVECs) were incubated with plasma from healthy pregnant (HP) and PE women; NO quantification was assessed by a fluorescence compound. We found that endothelial cells incubated with plasma from women with PE show lower NO levels compared with the HP group (p < 0.0001). However, NEB treatment increases NO levels, partially, mediated by β3 adrenergic receptors (p < 0.0001) and through eNOS activation (p < 0.0001). Conclusions: Our results suggest that NEB acts in NO synthesis through eNOS activation and β3 adrenergic receptors in the endothelium. However, further studies will be needed to understand this molecule.
Highlights
Nebivolol (NEB) is a third-generation beta-blocker combining highly selectivity for the β1 adrenoceptors and the ability to release nitric oxide (NO) through the endothelium [1]. It is a racemic mixture of two enantiomers, D- and L-nebivolol, where L-nebivolol behaves as a β3 adrenergic receptor agonist, increasing Ca+2 efflux into endothelial cells by activating eNOS and increasing NO bioavailability [2]
Our results suggest that NEB acts through eNOS activation and β3 adrenergic receptors
Our results suggest that NEB acts through eNOS activation and β3 adrene in the endothelial cells following exposure to plasma from preeclamptic patients
Summary
Nebivolol (NEB) is a third-generation beta-blocker combining highly selectivity for the β1 adrenoceptors and the ability to release nitric oxide (NO) through the endothelium [1]. It is a racemic mixture of two enantiomers, D- and L-nebivolol, where L-nebivolol behaves as a β3 adrenergic receptor agonist, increasing Ca+2 efflux into endothelial cells by activating eNOS and increasing NO bioavailability [2]. In the present study, we evaluated the effect of NEB addition on NO levels in endothelial cells incubated with plasma from healthy pregnant (HP) women and with PE in the presence of NEB. We investigated the molecular mechanisms of NEB in NO synthesis through activation of endothelial nitric oxide synthase and β3 adrenoceptors
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