Efeitos da glutationa sobre a reatividade vascular em artérias mesentéricas de resistência de ratas hipertensas

Abstract

Arterial hypertension represents the main risk condition for cardiopathologies, and its complications are mediated by several mechanisms, such as endothelial dysfunction, characterized by the low availability of nitric oxide and imbalance between factors of relaxation and constriction of arterioles. Oxidative stress (OS) is associated with endothelial dysfunction and hypertension, due to the excess production of reactive oxygen species (ROS). The antioxidant system is responsible for inhibiting or reducing oxidation reactions and fighting ROS and OS in our body. Thus, we investigated that the use of the antioxidant glutathione (GSH) could have a beneficial effect on essential hypertension associated with hormonal dysfunction. This study was approved by CEUA/UFES (nº23/2020). Spontaneously hypertensive rats (SHR) were divided into 4 groups: (1) Sham, (2) Sham+ GSH (treatment with 200 mg GSH/kg intraperitoneally for 21 days) (3) OVX (ovariectomy) and (4) OVX+GSH. Blood pressure was measured by tail plethysmography and dose-response curves were performed in mesenteric arteries of the SHR using phenylephrine and acetylcholine. Incubations were performed with L-NAME (Nω-nitro-L-arginine methyl ester-300 µM), which is one of the inhibitors of nitric oxide synthase (NOS) enzymes, and with indomethacin (INDO - 10 µM), a cyclooxygenase (COX) inhibitor. Vascular levels of NO and hydrogen peroxide were determined in situ using the DAF-2 and DCF probe, respectively. Data were analyzed by one-way or two-way ANOVA, followed by the post-hoc Bonferroni/Tukey test. It was considered p < 0.05. The results found were that the treatment with GSH did not improve hemodynamic parameters, body weight or modify the resistance vessel reactivity of SHR animals to reverse hypertension, however it was observed that GSH may be able to improve and maintain vasodilation when NO is attenuated. We suggest that GSH may exert a modulatory effect on endothelial mediators and potentiate vasodilation in ovariectomized SHR rats.