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

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Victoria M Youngblood ◽  
Ana QG da Silva ◽  
Laura C Duling ◽  
Nancy L Kanagy
Keyword(s):  
Reactive Oxygen Species ◽  
Sleep Apnea ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induced Hypertension

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.

scholarly journals Reactive Oxygen Species Production in Peripheral Blood Neutrophils of Obstructive Sleep Apnea Patients

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Guoda Pilkauskaite ◽  
Skaidrius Miliauskas ◽  
Raimundas Sakalauskas
Keyword(s):  
Reactive Oxygen Species ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Peripheral Blood ◽  
Reactive Oxygen ◽  
Apnea Hypopnea Index ◽  
Ros Production ◽  
Oxygen Species ◽  
Obstructive Sleep ◽  
Blood Neutrophils

Obstructive sleep apnea (OSA) as well as obesity is associated with increased production of reactive oxygen species (ROS). Neutrophils produce great amounts of ROS. The aim was to evaluate peripheral blood neutrophils ROS production in men with OSA and to establish relations with disease severity and obesity.Methods. Forty-six men with OSA and 10 controls were investigated. OSA was confirmed by polysomnography (PSG), when apnea/hypopnea index was >5/h. Body mass index (BMI) was evaluated. Neutrophils were isolated from peripheral blood in the morning after PSG. Dihydrorhodamine-123 was used for ROS detection. Data is presented as median (25th and 75th percentiles). All subjects were divided into four groups: nonobese mild-to-moderate OSA, obese mild-to-moderate OSA, nonobese severe OSA, and obese severe OSA.Results. Neutrophil ROS production was higher in nonobese severe OSA group compared to nonobese mild-to-moderate OSA (mean fluorescence intensity (MFI) 213.4 (89.0–238.9) versus 44.5 (20.5–58.4),P<0.05). In obese patient groups, ROS production was more increased in severe OSA compared to mild-to-moderate OSA group (MFI 74.5 (47.9–182.4) versus 31.0 (14.8–53.8),P<0.05). It did not differ in the groups with different BMI and the same severity of OSA.Conclusion. Increased neutrophil ROS production was related to more severe OSA but not obesity.

scholarly journals Vascular smooth muscle Jak2 mediates angiotensin II-induced hypertension via increased levels of reactive oxygen species

2011 ◽  
Vol 91 (1) ◽  
pp. 171-179 ◽  
Author(s):  
Annet Kirabo ◽  
Patrick N. Kearns ◽  
Yagna P. Jarajapu ◽  
Jennifer M. Sasser ◽  
Suk Paul Oh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
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.

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