Progesterone induced blocking factor improves blood pressure, mitochondrial dysfunction and reactive oxygen species in response to sFlt‐1 induced hypertension during pregnancy

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Evangeline Deer ◽  
Jalisa Jones ◽  
Kyliegh Comely ◽  
Denise C. Cornelius ◽  
Tarek Ibrahim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Blocking Factor ◽  
Induced Hypertension

scholarly journals NaHS or Lovastatin Attenuates Cyclosporine A–Induced Hypertension in Rats by Inhibiting Epithelial Sodium Channels

2021 ◽  
Vol 12 ◽  
Author(s):  
Qiu-Shi Wang ◽  
Chen Liang ◽  
Shuai Jiang ◽  
Di Zhu ◽  
Yu Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Cyclosporine A ◽  
Reactive Oxygen ◽  
Kidney Cortex ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Open Probability ◽  
Induced Hypertension ◽  
Intracellular Cholesterol

The use of cyclosporine A (CsA) in transplant recipients is limited due to its side effects of causing severe hypertension. We have previously shown that CsA increases the activity of the epithelial sodium channel (ENaC) in cultured distal nephron cells. However, it remains unknown whether ENaC mediates CsA-induced hypertension and how we could prevent hypertension. Our data show that the open probability of ENaC in principal cells of split-open cortical collecting ducts was significantly increased after treatment of rats with CsA; the increase was attenuated by lovastatin. Moreover, CsA also elevated the levels of intracellular cholesterol (Cho), intracellular reactive oxygen species (ROS) via activation of NADPH oxidase p47phox, serum- and glucocorticoid-induced kinase isoform 1 (Sgk1), and phosphorylated neural precursor cell–expressed developmentally downregulated protein 4–2 (p-Nedd4-2) in the kidney cortex. Lovastatin also abolished CsA-induced elevation of α-, ß-, and γ-ENaC expressions. CsA elevated systolic blood pressure in rats; the elevation was completely reversed by lovastatin (an inhibitor of cholesterol synthesis), NaHS (a donor of H2S which ameliorated CsA-induced elevation of reactive oxygen species), or amiloride (a potent ENaC blocker). These results suggest that CsA elevates blood pressure by increasing ENaC activity via a signaling cascade associated with elevation of intracellular ROS, activation of Sgk1, and inactivation of Nedd4-2 in an intracellular cholesterol-dependent manner. Our data also show that NaHS ameliorates CsA-induced hypertension by inhibition of oxidative stress.

scholarly journals Reactive oxygen species contribute to sleep apnea-induced hypertension in rats

2007 ◽  
Vol 293 (5) ◽  
pp. H2971-H2976 ◽  
Author(s):  
Carmen M. Troncoso Brindeiro ◽  
Ana Q. da Silva ◽  
Kyan J. Allahdadi ◽  
Victoria Youngblood ◽  
Nancy L. Kanagy
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Sleep Apnea ◽  
Arterial Pressure ◽  
Reactive Oxygen ◽  
Mesenteric Arteries ◽  
Plain Water ◽  
Oxygen Species ◽  
Induced Hypertension

In clinical studies, sleep apnea is associated with hypertension, oxidative stress, and increased circulating endothelin-1 (ET-1). We previously developed a model of sleep apnea by exposing rats to eucapnic intermittent hypoxia (IH-C) during sleep, which increases both blood pressure and plasma levels of ET-1. Because similar protocols in mice increase tissue and plasma markers of oxidative stress, we hypothesized that IH-C generation of reactive oxygen species (ROS) contributes to the development of ET-1-dependent hypertension in IH-C rats. To test this, male Sprague-Dawley rats were instrumented with indwelling blood pressure telemeters and drank either plain water or water containing the superoxide dismutase mimetic, Tempol (4-hydroxy-2,2,6,6-tetramethyl-piperidine-1-oxyl, 1 mM). Mean arterial pressure (MAP) and heart rate (HR) were recorded for 3 control days and 14 treatment days with rats exposed 7 h/day to IH-C or air/air cycling (Sham). On day 14, MAP in IH-C rats treated with Tempol (107 ± 2.29 mmHg) was significantly lower than in untreated IH-C rats (118 ± 9 mmHg, P < 0.05). Tempol did not affect blood pressure in sham-operated rats (Tempol = 101 ± 3, water = 101 ± 2 mmHg). Immunoreactive ET-1 was greater in plasma from IH-C rats compared with plasma from sham-operated rats but was not different from Sham in Tempol-treated IH-C rats. Small mesenteric arteries from IH-C rats but not Tempol-treated IH-C rats had increased superoxide levels as measured by ferric cytochrome c reduction, lucigenin signaling, and dihydroethidium fluorescence. The data show that IH-C increases ET-1 production and vascular ROS levels and that scavenging superoxide prevents both. Thus oxidative stress appears to contribute to increases in ET-1 production and elevated arterial pressure in this rat model of sleep apnea-induced hypertension.

Butin reduces oxidative stress-induced mitochondrial dysfunction via scavenging of reactive oxygen species

2010 ◽  
Vol 48 (3) ◽  
pp. 922-927 ◽  
Author(s):  
Rui Zhang ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Weon Young Chang ◽  
Young Hee Maeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Danshenol A Alleviates Hypertension-Induced Cardiac Remodeling by Ameliorating Mitochondrial Dysfunction and Suppressing Reactive Oxygen Species Production

2019 ◽  
Vol 2019 ◽  
pp. 1-18
Author(s):  
Kai Chen ◽  
Yiqing Guan ◽  
Yunci Ma ◽  
Dongling Quan ◽  
Jingru Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Spontaneously Hypertensive Rat ◽  
Cardiac Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Spontaneously Hypertensive ◽  
Underlying Mechanisms

Current therapeutic approaches have a limited effect on cardiac remodeling, which is characteristic of cardiac fibrosis and myocardial hypertrophy. In this study, we examined whether Danshenol A (DA), an active ingredient extracted from the traditional Chinese medicine Radix Salviae, can attenuate cardiac remodeling and clarified the underlying mechanisms. Using the spontaneously hypertensive rat (SHR) as a cardiac remodeling model, DA ameliorated blood pressure, cardiac injury, and myocardial collagen volume and improved cardiac function. Bioinformatics analysis revealed that DA might attenuate cardiac remodeling through modulating mitochondrial dysfunction and reactive oxygen species. DA repaired the structure/function of the mitochondria, alleviated oxidative stress in the myocardium, and restored apoptosis of cardiomyocytes induced by angiotensin II. Besides, DA inhibited mitochondrial redox signaling pathways in both the myocardium and cardiomyocytes. Thus, our study suggested that DA attenuates cardiac remodeling induced by hypertension through modulating mitochondrial dysfunction and reactive oxygen species.

scholarly journals Rosmarinic acid induces programmed cell death in Arabidopsis seedlings through reactive oxygen species and mitochondrial dysfunction

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208802 ◽  
Author(s):  
Fabrizio Araniti ◽  
Aitana Costas-Gil ◽  
Luz Cabeiras-Freijanes ◽  
Antonio Lupini ◽  
Francesco Sunseri ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Dysfunction ◽  
Rosmarinic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species
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