Isolated Natural Antioxidants as a new Possible Therapeutic Alternative for the Treatment of Hypertension.

Oxidative stress is one of the main mechanisms involved in the pathophysiology of arterial hypertension, inducing direct effects on the vasculature, and contributing to endothelial dysfunction and consequent impairment of vascular relaxation. Despite a large number of pharmacological treatments available, intolerable side effects are reported, which makes the use of natural antioxidants a promising and complementary alternative for the prevention and treatment of hypertension. From this perspective, the current review aims to investigate and characterize the main antioxidants of natural origin for the treatment of hypertension. Antioxidants act in the inhibition or extinction of chemical reactions involving free radicals and consequently reduce the occurrence of damage caused by these cellular components. The main natural antioxidants for treating hypertension include caffeic acid, ferulic acid, curcumin, apocynin, quercetin, lipoic acid, and lycopene. The effects associated with these antioxidants, which make them therapeutic targets for decreasing high blood pressure, include increased activation of antioxidant enzymes, stimulation of nitric oxide bioavailability, and reduction in angiotensin-converting enzyme activity, arginase, and NADPH oxidase, whose effects contribute to reducing oxidative stress, improving endothelial function, and preventing cardiovascular dysfunctions. Thus, several products with antioxidant properties that are available in nature and their application in the treatment of hypertension are described in the literature. The therapeutic effects of these products seem to regulate several parameters related to arterial hypertension, in addition to combating and preventing the deleterious effects related to the disease.

Involvement of shedding induced by ADAM17 on the nitric oxide pathway in hypertension.

A Disintegrin and Metalloprotease 17 (ADAM17), also called tumor necrosis factor-ɑ (TNF-ɑ) convertase (TACE), is a well-known protease involved in the sheddase of growth factors, chemokines and cytokines. ADAM17 is also enrolled in hypertension, especially by shedding of angiotensin converting enzyme type 2 (ACE2) leading to impairment of angiotensin 1-7 [Ang-(1-7)] production and injury in vasodilation, induction of renal damage and cardiac hypertrophy. Activation of Mas receptor (MasR) by binding of Ang-(1-7) induces an increase in the nitric oxide (NO) gaseous molecule, which is an essential factor of vascular homeostasis and blood pressure control. On the other hand, TNF-ɑ has demonstrated to stimulate a decrease in nitric oxide bioavailability, triggering a disrupt in endothelium-dependent vasorelaxation. In spite of the previous studies, little knowledge is available about the involvement of the metalloprotease 17 and the NO pathways. Here we will provide an overview of the role of ADAM17 and Its mechanisms implicated with the NO formation.