Arq. Bras. Cardiol. 2024; 121(12): e20240836
Nitrite Supplementation Attenuates Vascular Stiffness Independently of Physical Exercise
Alex Yuiti Ogura
, Claudiane Maria Barbosa
, Silvio Assis de Oliveira Junior
This Short Editorial is referred by the Research article "Short-term Oral Nitrite Administration Decreases Arterial Stiffness in Both Trained and Sedentary Wistar Rats".
Exercise training is considered one of the most efficient non-pharmacological measures for reducing blood pressure and increasing the redox state in blood vessel walls. Indeed, regular exercise training can cause endothelial relaxation by increasing nitric oxide (NO) levels, with or without a reduction in the amount of reactive oxygen species (ROS). Excessive production and/or accumulation of ROS can result in redox imbalance, with decreased NO bioavailability and consequent endothelial dysfunction., In this regard, reduced NO release is one of the critical factors for the development of systemic arterial hypertension.,
Importantly, NO is a diatomic gaseous signaling molecule that is water-soluble and can freely pass through the cell membrane. This peptide is essential in the regulation of several physiological actions in the body, being of utmost importance for vasodilation, immune response, neurotransmission, apoptosis, and genetic regulation. When released, NO diffuses from endothelial cells to vascular smooth muscle cells, promoting relaxation and vasodilation. Through this mechanism, NO can reduce vascular peripheral resistance and, consequently, decrease blood pressure. In the endogenous context, NO production results from the oxidation and cleavage of the guanidine group of L-arginine, with the release of NO and L-citrulline. Then, free NO is easily transformed into nitrite and nitrate, the current products are later recycled into NO and other forms of nitrogen oxidation, through the nitrate/nitrite/NO pathway.
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