Hypertension caused by chronic intermittent hypoxia – influence of chemoreceptors and sympathetic nervous system

Leßke, J.; Fletcher, Eugene C.; Bao, Gang; Unger, Thomas

doi:10.1097/00004872-199715120-00060

Cited by 244 publications

(232 citation statements)

References 53 publications

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“…This is strikingly similar to the effects of chronic exposure to IH in adults, which also induces hypertension (12). In adults, this depends on the recurrent activation of peripheral chemoreceptors and is prevented by bilateral carotid body denervation during exposure (12,30), and following chemical sympathetic denervation (13). This is accompanied by an enhanced activity of peripheral chemoreceptors (23,48), chronic sympathetic activation (11,29,31,44), blunted baroreflex responses (3,31), and functional changes in the vascular bed (7).…”

Section: Respiratory and Hemodynamic Variables In Normoxia In Controlmentioning

confidence: 64%

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Julien

Niane

Kinkead

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Julien CA, Niane L, Kinkead R, Bairam A, Joseph V. Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia. Am J Physiol Regul Integr Comp Physiol 299: R192-R205, 2010. First published April 21, 2010 doi:10.1152/ajpregu.00707.2009.-We tested the hypothesis that exposure to neonatal intermittent hypoxia (n-IH) in rat pups alters central integrative processes following acute and intermittent peripheral chemoreceptor activation in adults. Newborn male rats were exposed to n-IH or normoxia for 10 consecutive days after birth. We then used both awake and anesthetized 3-to 4-mo-old rats to record ventilation, blood pressure, and phrenic and splanchnic nerve activities to assess responses to peripheral chemoreflex activation (acute hypoxic response) and long-term facilitation (LTF, long-term response after intermittent hypoxia). In anesthetized rats, phrenic and splanchnic nerve activities and hypoxic responses were also recorded with or without intact carotid body afferent signal (bilateral chemodenervation) or in response to electrical stimulations of the carotid sinus nerve. In awake rats, n-IH alters the respiratory pattern (higher frequency and lower tidal volume) and increased arterial blood pressure in normoxia, but the ventilatory response to repeated hypoxic cycles was not altered. In anesthetized rats, phrenic nerve responses to repeated hypoxic cycles or carotid sinus nerve stimulation were not altered by n-IH; however, the splanchnic nerve response was suppressed by n-IH compared with control. In control rats, respiratory LTF was apparent in anesthetized but not in awake animals. In n-IH rats, respiratory LTF was not apparent in awake and anesthetized animals. Following intermittent electrical stimulation, however, phrenic LTF was clearly present in n-IH rats, being similar in magnitude to controls. We conclude that, in adult n-IH rats: 1) arterial blood pressure is elevated, 2) peripheral chemoreceptor responses to hypoxia and its central integration are not altered, but splanchnic nerve response is suppressed, 3) LTF is suppressed, and 4) the mechanisms involved in the generation of LTF are still present but are masked most probably as the result of an augmented inhibitory response to hypoxia in the central nervous system. neonatal intermittent hypoxia; long-term facilitation DEVELOPMENT OF THE RESPIRATORY control system is tightly regulated by complex interactions between genetic and environmental factors that contribute to shape the mature phenotypic expression of this neural network (4). Over the past years, several studies have documented that alterations in environmental oxygen levels during development lead to important changes of the respiratory control system (4). A particular importance has been given to intermittent hypoxic exposure (38, 47, 50) because it may be used in laboratory animals to reproduce some of the effects encountered in human newborn suffering from apneas, which remains one of the major cause...

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Section: Respiratory and Hemodynamic Variables In Normoxia In Controlmentioning

confidence: 64%

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Julien

Niane

Kinkead

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Animal studies in rats and dogs have identified possible mechanisms by which OSA might lead to hypertension such as intermittent hypoxemia, chemoreceptor stimulation, 136 sympathetic activation, 136,137 and the renin-angiotensin system. In dogs, obstructing a tracheostomy to simulate apnea causes an acute increase in BP of Ϸ20 mm Hg, which persists for several hours and is exacerbated by prior sleep deprivation.…”

Section: Osa and The Origin And Progression Of Hypertensionmentioning

confidence: 99%

Sleep Apnea and Cardiovascular Disease

et al. 2008

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“…The hypertensive effect of chronic intermittent hypoxia outlasts hypoxemia in animal models. [4,5] Morgan et al demonstrated in healthy volunteers that hypoxic hypercapnia leads to a protracted increase in MSA, whereas hyperoxic hypercapnia only transiently increases sympathetic activity indicating that hypoxemia is responsible for the effect. [40] Chronic intermittent hypoxia has thus clinically relevant prolonged effects on blood pressure in animal models.…”

Section: Discussionmentioning

confidence: 99%

“…In a rat model, repetitive periods of hypoxia over 30 days caused hypertension persisting beyond the exposure to intermittent hypoxia. [4] In dogs, hypoxic episodes due to repetitive airway obstruction during sleep resulted in acute transient increases in nighttime blood pressure and eventually provoked a sustained daytime hypertension. [5] It is likely that the same mechanisms are valid in humans too, since obstructive sleep apnea leads to increased SNS activity and increased daytime blood pressure.…”

Section: Introductionmentioning

confidence: 99%

Spontanous periodic breathing is associated with sympathetic hyperreactivity and baroreceptor dysfunction in hypertension

Binggeli

Sudano²,

Corti³

et al. 2010

Journal of Hypertension

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OBJECTIVES: Intermittent periods of hypoxemia such as during periodic breathing are associated with hypertension and increased sympathetic activity. In patients with sleep apnea syndrome, hypertension is common. Treating apnea improves hypertension and reduces sympathetic outflow. The aim of the present study was to investigate the phenomenon and mechanisms of spontaneous periodic breathing in patients with hypertension. METHOD: We examined 43 hypertensive patients with untreated hypertension without left-ventricular dysfunction, heart failure or sleep apnea syndrome. Muscle sympathetic nerve activity (MSA), heart rate (HR), blood pressure (BP) and respiration were continuously recorded at rest and during cold-pressor testing. Oxygen and a CO2-enriched gas were used to test central and peripheral chemoreceptors, respectively. Baroreceptor gain was measured using the alpha method. RESULTS: Seven out of 43 patients showed spontaneous periodic breathing while awake. No difference in MSA, HR and BP was seen between patients with and without periodic breathing at rest except the breathing pattern. However, the cold-pressor test caused a larger increase of MSA in patients with periodic breathing (203 +/-62 vs. 62 +/-8%, P < 0.0001 by ANOVA), as well as systolic (46 +/-6 vs. 25 +/-3 mmHg, P = 0.002) and diastolic BP (26 +/-5 vs. 12 +/-1 mmHg, P = 0.004, ANOVA). Baroreceptor gain was markedly higher in patients with periodic breathing. Chemoreceptor sensitivity was comparable. CONCLUSION: Spontaneous periodic breathing is relatively common in patients with hypertension and is associated with greatly enhanced responses to cold-pressor testing. We suggest increased baroreceptor gain and sympathetic outflow as a cause for the oscillatory respiration pattern via barorespiratory coupling.

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Hypertension caused by chronic intermittent hypoxia – influence of chemoreceptors and sympathetic nervous system

Cited by 244 publications

References 53 publications

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Sleep Apnea and Cardiovascular Disease

Spontanous periodic breathing is associated with sympathetic hyperreactivity and baroreceptor dysfunction in hypertension

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