Sensory plasticity of carotid body is correlated with oxidative stress in paraventricular nucleus during chronic intermittent hypoxia

Chronic intermittent hypoxia (CIH), main feature of obstructive sleep apnea, produces nitro-oxidative stress, which contributes to potentiate carotid body (CB) chemosensory discharges and sympathetic-adrenal-axis activity, leading to hypertension. The MnSOD enzymatic activity, a key enzyme on oxidative stress control, is reduced by superoxide-induced nitration. However, the effects of CIH-induced nitration on MnSOD enzymatic activity in the CB and adrenal gland are not known. We studied the effects of CIH on MnSOD protein and immunoreactive (MnSOD-ir) levels in the CB, adrenal gland and superior cervical ganglion (SCG), and on 3-nitrotyrosine (3-NT-ir), CuZnSOD (CuZnSOD-ir), MnSOD nitration, and its enzymatic activity in the CB and adrenal gland from male Sprague-Dawley rats exposed to CIH for 7 days. CIH increased 3-NT-ir in CB and adrenal gland, whereas MnSOD-ir increased in the CB and in adrenal cortex, but not in the whole adrenal medulla or SCG. CIH nitrated MnSOD in the CB and adrenal medulla, but its activity decreased in the adrenal gland. CuZnSOD-ir remained unchanged in both tissues. All changes observed were prevented by ascorbic acid treatment. Present results show that CIH for 7 days produced MnSOD nitration, but failed to reduce its activity in the CB, because of the increased protein level.

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Elevated Oxidative Stress and Inflammation in Hypothalamic Paraventricular Nucleus Are Associated With Sympathetic Excitation and Hypertension in Rats Exposed to Chronic Intermittent Hypoxia

Frontiers in Physiology ◽

10.3389/fphys.2018.00840 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 13

Author(s):

Tiejun Li ◽

Yanli Chen ◽

Chaojun Gua ◽

Baogang Wu

Keyword(s):

Oxidative Stress ◽

Paraventricular Nucleus ◽

Intermittent Hypoxia ◽

Hypothalamic Paraventricular Nucleus ◽

Chronic Intermittent Hypoxia

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Role of oxidative stress-induced endothelin-converting enzyme activity in the alteration of carotid body function by chronic intermittent hypoxia

Experimental Physiology ◽

10.1113/expphysiol.2013.073700 ◽

2013 ◽

Vol 98 (11) ◽

pp. 1620-1630 ◽

Cited By ~ 29

Author(s):

Ying-Jie Peng ◽

Jayasri Nanduri ◽

Gayatri Raghuraman ◽

Ning Wang ◽

Ganesh K. Kumar ◽

...

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Carotid Body ◽

Intermittent Hypoxia ◽

Chronic Intermittent Hypoxia ◽

Converting Enzyme ◽

Body Function ◽

Endothelin Converting Enzyme

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Chronic intermittent hypoxia-induced vascular enlargement and VEGF upregulation in the rat carotid body is not prevented by antioxidant treatment

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00128.2011 ◽

2011 ◽

Vol 301 (5) ◽

pp. L702-L711 ◽

Cited By ~ 24

Author(s):

Rodrigo Del Rio ◽

Cristian Muñoz ◽

Paulina Arias ◽

Felipe A. Court ◽

Esteban A. Moya ◽

...

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Carotid Body ◽

Intermittent Hypoxia ◽

Vessel Diameter ◽

Chronic Intermittent Hypoxia ◽

Sprague Dawley ◽

Antioxidant Treatment ◽

Sprague Dawley Rats ◽

Vascular Area

Chronic intermittent hypoxia (CIH), a characteristic of sleep obstructive apnea, enhances carotid body (CB) chemosensory responses to hypoxia, but its consequences on CB vascular area and VEGF expression are unknown. Accordingly, we studied the effect of CIH on CB volume, glomus cell numbers, blood vessel diameter and number, and VEGF immunoreactivity (VEGF-ir) in male Sprague-Dawley rats exposed to 5% O2, 12 times/h for 8 h or sham condition for 21 days. We found that CIH did not modify the CB volume or the number of glomus cells but increased VEGF-ir and enlarged the vascular area by increasing the size of the blood vessels, whereas the number of the vessels was unchanged. Because oxidative stress plays an essential role in the CIH-induced carotid chemosensory potentiation, we tested whether antioxidant treatment with ascorbic acid may impede the vascular enlargement and the VEGF upregulation. Ascorbic acid, which prevents the CB chemosensory potentiation, failed to impede the vascular enlargement and the increased VEGF-ir. Thus present results suggest that the CB vascular enlargement induced by CIH is a direct effect of intermittent hypoxia and not secondary to the oxidative stress. Accordingly, the subsequent capillary changes may be secondary to the mechanisms involved in the neural chemosensory plasticity induced by intermittent hypoxia.

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