Physiological basis for a causal relationship of obstructive sleep apnoea to hypertension

Weiss, J. Woodrow; Liu, M. D. Yuzhen; Huang, Jianxiang

doi:10.1113/expphysiol.2006.035733

Cited by 65 publications

(59 citation statements)

References 47 publications

(53 reference statements)

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“…A inativação do óxido nítrico pelos radicais livres de oxigênio e a ativação dos receptores de angiotensina II e tromboxane A2 (TXA 2 ) aumentam a geração de endotelina-1 (ET-1) e podem ocasionar vasoconstrição e disfunção endotelial (34). Além disso, a vasodilatação independente do endotélio também se mostrou comprometida nos pacientes com AOS, conforme foi demonstrado por Kato e cols.…”

Contribuição da apnéia obstrutiva do sono para o estresse oxidativo da obesidade

Lima

Franco

Castro

et al. 2008

Arq Bras Endocrinol Metab

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RESUMOObjetivo: O objetivo do trabalho foi verificar a influência da apnéia obstrutiva do sono (AOS) sobre o estresse oxidativo da obesidade e o efeito do pressão positiva de vias aéreas (CPAP) nestes pacientes. Métodos: Os pacientes com IMC 30 kg/m 2 foram divididos em: a) grupo 1: dez indivíduos sem AOS; b) grupo 2: dez portadores de AOS que não fizeram o uso do CPAP; e c) grupo 3: nove portadores de AOS que fizeram uso do CPAP durante dois meses. Resultados: O grupo 3 apresentou, após o uso do CPAP, redução na produção de superóxido (SO) [13,2 (10,3-19,6) versus 10,5 (5,8-11,8) ABSTRACTObstructive Sleep Apnea Contribution to Oxidative Stress in Obesity. Objective: The aim of this paper was to check the influence of obstructive sleep apnea (OSA) on obesity oxidative stress and CPAP (Continuous Positive Airway Pressure) effect on oxidative stress and in these patients. Methods: Twenty nine male patients considered obese (BMI 30kg/m 2 ) were divided into 3 groups: a) Group I: 10 OSA free patients (apnea-hipopnea index (AHI) 5); b) Group 2: 10 with moderate to serious OSA (AHI 20); c) Group 3: 9 with OSA from moderate to serious (AHI 20) using CPAP,, minimum 4 hours/ night for 2 months. Results: Significant differences before and after CPAP usage were observed in group 3 in the following variables: reduction of superoxide (SO) production [13,2 (10,3-19,6) vs. 10,5 (5,8-11,8) nmoles O 2 -/2x106 PMN] and increase in serum nitrite/nitrates levels [24,5 (16,7-33,5) vs. 49,5 (39,3-58,1) M]. Positive correlation between Apnea-Hypopnea Index (AHI) and SO (r = 0,726) and negative correlation was observed between AHI and serum nitrite/nitrates levels (r = 0,867

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Contribuição da apnéia obstrutiva do sono para o estresse oxidativo da obesidade

Lima

Franco

Castro

et al. 2008

Arq Bras Endocrinol Metab

View full text Add to dashboard Cite

show abstract

“…[293][294][295][296][297][298][299] Together these processes conspire to produce renal fibrosis and sustained hypertension and their associated means of reducing renal oxygenation ( figure 1). 82,[300][301][302][303][304] Oxygenation is further compromised by nocturnal hypoxia altering parasympathetic control of heart rate and inducing left ventricular hypertrophy. 305, 306 An additional consequence of sleep apnea is that it activates nuclear factor κB, initiating a cascade of events that include increased production of tumor necrosis factor α, interleukin 6, interleukin 8, interleukin 18, C-reactive protein, and C-C motif ligand 2.…”

Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

120

108

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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“…Indeed, in the last years, the proposal that the CB is involved in the progression of the CIH-induced hypertension received further attention . 3,4,7,18,21,22 Neural recordings of CB chemosensory activity have shown that CIH selectively Abstract-Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors.…”

mentioning

confidence: 99%

Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats

et al. 2016

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The obstructive sleep apnea (OSA), a worldwide sleep breathing disorder that affect 9% of women and 24% of adult men, 1 is an independent risk factor for systemic hypertension and stroke and is associated with atrial arrhythmogenesis. [2][3][4][5][6] Chronic intermittent hypoxia (CIH), which is the principal feature of OSA, is considered the main factor for the hypertension.2-4,7 CIH produces autonomic dysfunction characterized by sympathetic hyperactivity, alterations of heart rate (HR) variability (HRV), and reduction of cardiac baroreflex efficiency. [8][9][10][11][12][13][14] Although the link between OSA and hypertension is well established, the mechanisms responsible for the autonomic imbalance and the hypertension are not entirely known. CIH produces oxidative stress, inflammation, and endothelial dysfunction that contribute to the hypertension. [2][3][4]7 However, a growing body of evidences suggests that the carotid body (CB), the main oxygen chemoreceptor organ, 15 plays a crucial role in the development of autonomic alterations and hypertension after CIH. Indeed, patients with OSA and animals exposed to CIH show enhanced cardiorespiratory and sympathetic responses to hypoxia, suggesting that CIH potentiates the CB-mediated chemoreflex drive. 7,13,[16][17][18][19] found that bilateral CB denervation before the CIH exposure prevents the development of the hypertension in rats. Despite this important result, the idea that the CB chemoreceptor contributes to the progression of cardiovascular pathologies associated with OSA was not seriously considered until the last decade. Indeed, in the last years, the proposal that the CB is involved in the progression of the CIH-induced hypertension received further attention . 3,4,7,18,21,22 Neural recordings of CB chemosensory activity have shown that CIH selectively Abstract-Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors. Male Sprague-Dawley rats were exposed to control (Sham) conditions for 7 days and then to CIH (5% O 2 , 12/h 8 h/d) for a total of 28 days. At 21 days of CIH exposure, rats underwent bilateral CB ablation and then exposed to CIH for 7 additional days. Arterial blood pressure and ventilatory chemoreflex response to hypoxia were measured in conscious rats. In addition, cardiac autonomic imbalance, cardiac baroreflex gain, and arrhythmia score were assessed during the length of the experiments.In separate experimental series, we measured extracellular matrix remodeling content in cardiac atrial tissue and systemic oxidative stress. CIH induced hypertension, enhanced ventilatory response to hypoxia, induced autonomic imbalance toward sympathetic preponderance, reduced baroreflex gain, and inc...

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Physiological basis for a causal relationship of obstructive sleep apnoea to hypertension

Cited by 65 publications

References 47 publications

Contribuição da apnéia obstrutiva do sono para o estresse oxidativo da obesidade

Contribuição da apnéia obstrutiva do sono para o estresse oxidativo da obesidade

Hypoxia: The Force that Drives Chronic Kidney Disease

Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats

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