Cardiovascular risk and the effect of nitric oxide synthase inhibition in female rats: The role of estrogen

Castardo-de-Paula, Jaqueline C; Campos, Blenda Hyedra de; Amorim, Eric Diego Turossi; Silva, Rosiane V. da; Farias, Carine Coneglian de; Higachi, Luciana; Pinge‐Filho, Phileno; Barbosa, Décio Sabbatini; Martins‐Pinge, Marli Cardoso

doi:10.1016/j.exger.2017.07.016

Cited by 19 publications

(26 citation statements)

References 54 publications

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“…Another study documented that it has the ability to protect NO against its degradation by free radicles (Fabricio et al, ). All previous changes in serum levels of NO, catalase and lipid peroxides in OVX rats confirmed the occurrence of systemic oxidative stress which agreed with the increased MAP occurring at the end of the study in OVX‐group relative to the SC‐group which was in agreement with several studies (Al‐Bazii, ; Castardo‐de‐Paula et al, ).…”

Section: Discussionsupporting

confidence: 91%

Effect of experimentally induced hypertension on cerebellum of postmenopausal rat

El‐Tahawy

Hafez

Ramzy

et al. 2018

Journal Cellular Physiology

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Cerebellum seems to be a specific target for both the decrease of estrogen and hypertension in menopause. The aim of this study was to investigate the hypertension and menopause‐induced changes in rat’s cerebellar cortex and the possible mechanisms of these changes. Rats were divided into four groups: the sham‐operated control (SC‐group), the ovariectomized (OVX‐group), the hypertensive (H‐group), and the ovariectomized‐hypertensive (OVX‐H‐group) group. The mean arterial pressure (MAP), serum nitric oxide (NO), lipid peroxides and antioxidant catalase enzyme levels were assayed. Cerebellar tissue homogenization for analysis of lipid peroxides, antioxidant catalase enzyme, tumor necrosis factor‐α (TNF‐α), and estradiol was done. Quantification of adrenomedullin (AM) and interleukin‐10 (IL‐10) mRNA was also done. Cerebella were processed for histological, immunohistochemical and transmission electron microscopic examination. In the OVX‐group, insignificant structural and biochemical changes were observed compared with the SC‐group apart from the significantly increased lipid peroxides and decreased NO and catalase levels in serum. The H‐group showed an elevated lipid peroxides and TNF‐α levels, reduced catalase level, numerous degenerated Purkinje cells, vacuolations of the neuropil, some axonal degeneration, and few ghosts in the granular cell layer (GL). However, in OVX‐H‐group, oxidative stress, inflammation, and cerebellar damage were exacerbated and cerebellar estrogen was reduced associated with reduction in GL thickness and decreased Purkinje cells number. Most axoplasms had degenerated neurofilaments with abnormal myelination. The immunoexpression of glial fibrillary acidic protein were significantly increased in both OVX‐group and H‐group and significantly decreased in OVX‐H group. Gene expression of AM and IL‐10 were increased in cerebellar tissues of H‐group compared with the SC‐group but it was significantly decreased in OVX‐H‐group compared with H‐group. Taken together, postmenopausal rats with hypertension suffered from structural cerebellar changes than rats with only hypertension or estrogen deficiency separately due to augmentation of the increased oxidative stress markers and the proinflammatory cytokines (TNF‐α) with down regulation of the anti‐inflammatory cytokine (IL‐10) and the blood pressure regulator, AM. These suggested that high blood pressure is a critical factor for postmenopausal cerebellum.

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Section: Discussionsupporting

confidence: 91%

Effect of experimentally induced hypertension on cerebellum of postmenopausal rat

El‐Tahawy

Hafez

Ramzy

et al. 2018

Journal Cellular Physiology

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“…Provided that the L-NAME-mediated increase of mean arterial pressure was slight, the authors concluded that vasodilator status would arise from eNOS, whose activity is probably implicated in maintaining PON1 activity in ovariectomized rats. On the other hand, it was suggested that the higher increase in total plasma levels of NO in 17β-estradiol-treated rats was associated to iNOS activity [56].…”

Section: Vascular Effects Of Gonadal Hormonesmentioning

confidence: 99%

Mutual Influences between Nitric Oxide and Paraoxonase 1

2019

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One of the best consolidated paradigms in vascular pharmacology is that an uncontrolled excess of oxidizing chemical species causes tissue damage and loss of function in the endothelial and subendothelial layers. The fact that high-density lipoproteins play an important role in preventing such an imbalance is integrated into that concept, for which the expression and activity of paraoxonases is certainly crucial. The term paraoxonase (aryldialkyl phosphatase, EC 3.1.8.1) encompasses at least three distinct isoforms, with a wide variation in substrate affinity, cell and fluid localization, and biased expression of polymorphism. The purpose of this review is to determine the interactions that paraoxonase 1 has with nitric oxide synthase, its reaction product, nitric oxide (nitrogen monoxide, NO), and its derived reactive species generated in an oxidative medium, with a special focus on its pathological implications.

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“…There are three different isoforms of the NOS which produced by different genes with quite distinct localization, regulation, catalytic properties and inhibitor sensitivity. These isoforms are neuronal NOS & vascular endothelial NOS which are called the constitutive NOS isoforms (cNOS), and inducible NOS [6,7]. The constitutive NOS isoforms (cNOS) are calcium dependence, and they can be inhibited by the administration of L-NAME [6,7], while the inducible form of the NOSs is calcium independence, and its induction can be inhibited by treatment with glucocorticoids [5].…”

Section: Nitric Oxidementioning

confidence: 99%