Depressed baroreflex sensitivity in patients with obstructive sleep apnea.

Carlson, Jan; Hedner, Jan; Sellgren, Johan; Elam, Mikael; Wallin, B. G.

doi:10.1164/ajrccm.154.5.8912770

Cited by 216 publications

(135 citation statements)

References 26 publications

Supporting

Mentioning

117

Contrasting

Unclassified

Order By: Relevance

“…37 There is also a decrease in baroreceptor sensitivity in patients with long-term obstructive sleep apnea. 38 Our data indicate that altered chemoreflex activity is not an instigating factor for obesity-related hypertension.…”

Section: Baroreflexes But Not Chemoreflexes Become Aberrant In Early mentioning

confidence: 58%

Rapid Onset of Renal Sympathetic Nerve Activation in Rabbits Fed a High-Fat Diet

et al. 2012

View full text Add to dashboard Cite

Abstract-Hypertension and elevated sympathetic drive result from consumption of a high-calorie diet and deposition of abdominal fat, but the etiology and temporal characteristics are unknown. Rabbits instrumented for telemetric recording of arterial pressure and renal sympathetic nerve activity (RSNA) were fed a high-fat diet for 3 weeks then control diet for 1 week or control diet for 4 weeks. Baroreflexes and responses to air-jet stress and hypoxia were determined weekly. After 1 week of high-fat diet, caloric intake increased by 62%, accompanied by elevated body weight, blood glucose, plasma insulin, and leptin (8%, 14%, 134%, and 252%, respectively). Mean arterial pressure, heart rate, and RSNA also increased after 1 week (6%, 11%, and 57%, respectively). Whereas mean arterial pressure and body weight continued to rise over 3 weeks of high-fat diet, heart rate and RSNA did not change further. The RSNA baroreflex was attenuated from the first week of the diet. Excitatory responses to air-jet stress diminished over 3 weeks of high-fat diet, but responses to hypoxia were invariant. Resumption of a normal diet returned glucose, insulin, leptin, and heart rate to control levels, but body weight, mean arterial pressure, and RSNA remained elevated. In conclusion, elevated sympathetic drive and impaired baroreflex function, which occur within 1 week of consumption of a high-fat, high-calorie diet, appear integral to the rapid development of obesity-related hypertension. Increased plasma leptin and insulin may contribute to the initiation of hypertension but are not required for maintenance of mean arterial pressure, which likely lies in alterations in the response of neurons in the hypothalamus. Key Words: sympathetic nervous system Ⅲ obesity Ⅲ rabbits Ⅲ blood pressure Ⅲ heart rate O besity represents a significant risk for cardiovascular disease because of the relationship between excess body fat and hypertension. It is estimated that obesity contributes to hypertension in Ͼ60% of men and women entering the Framingham study.1 The mechanisms underlying this relationship are multifactorial, and for some time there was controversy as to whether the sympathetic nervous system was activated or inhibited in obesity-related hypertension. Bray 2 proposed that obesity was a result of low thermogenic activity secondary to low sympathetic activity, and certainly data from heart rate (HR) variability studies supported this hypothesis. Young and Landsberg 3 hypothesized that sympathetic outflow is increased in obesity to facilitate energy wastage by thermogenesis and to maintain body weight homeostasis, with elevated renal sympathetic activation and hypertension the sequelae. It is now clear that norepinephrine spillover to renal and skeletal muscle beds is increased in obese humans, 4 and microneurographic data indicate that skeletal muscle sympathetic nerve activity is greater in overweight humans, 5 consistent with the observation that sympathetic vasomotor activity in skeletal muscle is elevated in established obesity. 6,7 ...

show abstract

Section: Baroreflexes But Not Chemoreflexes Become Aberrant In Early mentioning

confidence: 58%

Rapid Onset of Renal Sympathetic Nerve Activation in Rabbits Fed a High-Fat Diet

et al. 2012

View full text Add to dashboard Cite

show abstract

“…An increase in plasma levels of norepinephrine associated with systolic arterial pressure was observed, suggesting a correlation between these factors and the development of the cardiovascular complications of obstructive sleep apnea syndrome 16 . The same authors pointed towards the decreased sensitivity of the baroreflex stimulus consequent to increased sympathetic activity as a possible mechanism for the development of sustained systemic arterial hypertension in patients with obstructive sleep apnea syndrome 17 . The recently published 4-year follow-up of 709 patients from an American working community supplied data for a first cohort study evaluating the obstructive sleep apnea syndrome as a risk factor for the development of arterial hypertension 2 .…”

Section: Discussionmentioning

confidence: 99%

Epworth's sleepiness scale in outpatients with different values of arterial blood pressure

Gus¹,

Silva²,

Fernandes³

et al. 2002

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

OBJECTIVE: To compare sleepiness scores of the Epworth scale in patients with different levels of arterial pressure when undergoing outpatient monitoring within the context of clinical evaluation. METHODS: A total of 157 patients selected for outpatient monitoring of arterial pressure during hypertension evaluation were divided into 3 groups: group 1 - normotensive; group 2 - hypertensive; group 3 - resistant hypertensive. For analysis, values > or = 11 were considered as associated with respiratory disturbances during sleep. RESULTS: Seventeen (10.8%) patients in group 1, 112 (71.3%) in group 2, and 28 (17.8%) in group 3, which was composed of aged, more severely hypertensive individuals, were analyzed. Groups were similar relative to sex and body mass index, but different in relation to systolic and diastolic pressure levels and age. Despite an absolute difference, no statistically significant difference occurred between Epworth scores and in the proportion of patients with values > or = 11 (5.9% vs. 18.8% vs. 212.4%; P=0.37). Despite the positive association between degree of sleepiness measured with the scale and the severity of the hypertension, no statistical significance occurred following control by age (p=0.18). CONCLUSION: A positive correlation exists between degree of sleepiness and hypertension severity. The absence of a statistical significance shown in the present study could be due to a beta type of error. Instruments that render this complaint into an objective finding could help in the pursuit of an investigation of respiratory disturbances during sleep in more severely hypertensive patients, and should therefore be studied better

show abstract

“…PaO 2 , arterial pressure in oxygen; PaCO 2 , arterial pressure in carbon dioxide; pHa, arterial pH; HCO 3 Ϫ , arterial bicarbonate concentration. P Ͻ 0.05 vs. control (*) and vs. baseline ( †).…”

Section: R196 Long-term Effects Of N-ih On Respiratory Ltfmentioning

confidence: 99%

“…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). Whether similar changes are also induced by exposure to neonatal hypoxia in newborns and have longlasting effects remains to be documented.…”

Section: Respiratory and Hemodynamic Variables In Normoxia In Controlmentioning

confidence: 99%

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

View full text Add to dashboard Cite

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...

show abstract

Depressed baroreflex sensitivity in patients with obstructive sleep apnea.

Cited by 216 publications

References 26 publications

Rapid Onset of Renal Sympathetic Nerve Activation in Rabbits Fed a High-Fat Diet

Rapid Onset of Renal Sympathetic Nerve Activation in Rabbits Fed a High-Fat Diet

Epworth's sleepiness scale in outpatients with different values of arterial blood pressure

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

Contact Info

Product

Resources

About