scholarly journals SP046RENAL SYMPATHETIC NERVE DENERVATION INHIBITS CHRONIC INTERMITTENT HYPOXIA-INDUCED HYPERTENSION BY DECREASING RENIN-ANGIOTENSIN SYSTEM AND OXIDATIVE STRESS IN A MOUSE MODEL OF SLEEP APNEA SYNDROME

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii120-iii120 ◽  
Author(s):  
Keiko Takahashi ◽  
Seiji Ueda ◽  
Takashi Kobayashi ◽  
Akira Nishiyama ◽  
Takeshi Sugaya ◽  
...  
2021 ◽  
Vol 320 (4) ◽  
pp. R519-R525
Author(s):  
Alexandria B. Marciante ◽  
Brent Shell ◽  
George E. Farmer ◽  
J. Thomas Cunningham

Sleep apnea is characterized by momentary interruptions in normal respiration and leads to periods of decreased oxygen, or intermittent hypoxia. Chronic intermittent hypoxia is a model of the hypoxemia associated with sleep apnea and results in a sustained hypertension that is maintained during normoxia. Adaptations of the carotid body and activation of the renin-angiotensin system may contribute to the development of hypertension associated with chronic intermittent hypoxia. The subsequent activation of the brain renin-angiotensin system may produce changes in sympathetic regulatory neural networks that support the maintenance of the hypertension associated with intermittent hypoxia. Hypertension and sleep apnea not only increase risk for cardiovascular disease but are also risk factors for cognitive decline and Alzheimer’s disease. Activation of the angiotensin system could be a common mechanism that links these disorders.


2007 ◽  
Vol 232 (11) ◽  
pp. 1409-1413 ◽  
Author(s):  
Carlo Selmi ◽  
Nicola Montano ◽  
Raffaello Furlan ◽  
Carl L. Keen ◽  
M. Eric Gershwin

2017 ◽  
Vol 22 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Olga Nikitidou ◽  
Euphemia Daskalopoulou ◽  
Aikaterini Papagianni ◽  
Vassilios Liakopoulos ◽  
Aikaterini Michalaki ◽  
...  

2015 ◽  
Vol 19 (4) ◽  
pp. 1205-1212 ◽  
Author(s):  
L. Sardo ◽  
P. Palange ◽  
F. Di Mario ◽  
B. Barbano ◽  
A. Gigante ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Ma ◽  
Yu-Ming Kang* ◽  
Zhi-Ming Yang ◽  
Joseph Francis*

Introduction: Neurohumoral mechanisms play an important role in the pathophysiology of congestive heart failure (HF). Recent studies suggest that the brain renin angiotensin system (RAS) plays an important role in regulating body fluids and sympathetic drive in HF. In addition, it has been shown that there is cross talk between cytokines and RAS in cardiovascular disease. In this study we determined whether blockade of brain RAS attenuate inflammatory cytokines and oxidative stress in HF rats. Methods and Results: Adult male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and subjected to coronary artery ligation to induce HF and confirmed by echocardiography. Rats were treated with an angiotensin type 1 receptors (AT1-R) antagonist losartan (LOS, 20 μg/hr, ICV) or vehicle (VEH) for 4 weeks. At the end of the study, left ventricular (LV) function was measured by echocardiography and rats were sacrificed, and brain and plasma samples were collected for measurements of cytokines and superoxide using immunohistochemistry, Western blot and real time RT-PCR. HF rats induced significant increases in Nuclear Factor-kappaB (NF-κB) p50-positive neurons and activated microglia in the paraventricular nucleus (PVN) of hypothalamus, and TNF-α, IL-1β, IL-6 and NF-κB p50 in hypothalamus when compared with sham rats. These animals also had increased staining for dihydroethidium (DHE) and plasma levels of norepinephrine (NE), an indirect indicator of sympathetic activity. In contrast, ICV treatment with LOS attenuated cytokine expression and oxidative stress in the PVN and hypothalamus when compared with VEH treated HF rats. ICV treatment with LOS also reduced plasma NE levels, and proinflammatory cytokine, heart weight to body weight ratio with decreased LV end-diastolic pressure. Conclusions : These findings suggest the cross talk between the cytokines and renin angiotensin system within the brain contribute to sympatho-excitation in HF.


Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1184 ◽  
Author(s):  
Peng Guan ◽  
Zhi-Min Sun ◽  
Li-Fei Luo ◽  
Ya-Shuo Zhao ◽  
Sheng-Chang Yang ◽  
...  

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.


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