Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

Linz, Dominik; Mahfoud, Felix; Schotten, Ulrich; Ukena, Christian; Neuberger, Hans‐Ruprecht; Wirth, Klaus; Böhm, Michael

doi:10.1161/hypertensionaha.112.191965

Cited by 201 publications

(134 citation statements)

References 35 publications

Supporting

Mentioning

126

Contrasting

Unclassified

Order By: Relevance

“…In a porcine model of obstructive sleep apnea (tracheal occlusion), renal denervation prevented the postapneic increase in blood pressure, attenuated the shortening in atrial effective refractory period, and decreased the ability to induce atrial fibrillation. 13 The study emphasizes the ability of renal denervation to modulate the autonomic control of the heart leading to a decrease in the generation of atrial arrhythmias during experimental obstructive sleep apnea.…”

Section: Selective Catheter-based Renal Sympathetic Denervationmentioning

confidence: 99%

Sympathetic Nervous System and Hypertension

2013

View full text Add to dashboard Cite

With the development and implementation of device-based therapeutic interventions to decrease renal and systemic nerve activity in patients with resistant hypertension, there has been an increase in research dealing with the role of the sympathetic nervous system in hypertension. These interventions have produced substantial decreases in blood pressure in patients wherein pharmacological treatments, including agents which inhibit the effects of the renin-angiotensin-aldosterone system, have failed serves to confirm and reassert the essential role of the sympathetic nervous system in hypertension. This review will encompass recent publications dealing with the sympathetic nervous system and hypertension, focusing on those recently published in Hypertension. Sympathetic Activation in Animal Models Obesity-Related HypertensionAlthough there has been a debate as to whether sympathetic activation is a cause or consequence of obesity, the studies noted below support the view that it is the obesity that leads to sympathetic activation. The importance of this sympathetic activation for the development of the hypertension is supported by the finding that renal denervation prevents the development of obesity hypertension in the dog.Studies have now focused on the developmental phase of obesity hypertension regarding the renal sympathoexcitation. In rabbits fed high-fat diets, body weight, plasma insulin and leptin concentrations, mean arterial pressure, heart rate, and renal sympathetic nerve activity were all increased after 1 week.1 Mean arterial pressure and body weight continued to increase over 3 weeks of high-fat diet, whereas heart rate and renal sympathetic nerve activity did not change further. Arterial baroreflex control of renal sympathetic nerve activity was attenuated from the first week of the high-fat diet. Excitatory responses to air jet stress diminished over 3 weeks of high-fat diet. Resumption of normal diet normalized glucose, insulin, leptin, and heart rate, but body weight, visceral fat content, mean arterial pressure, and renal sympathetic nerve activity remained elevated. Increased renal sympathetic nerve activity and its impaired baroreflex control, which occur with 1 week of high-fat feeding, seem integral to the rapid development of obesity hypertension. Increased plasma leptin and insulin may contribute to the initiation of hypertension but are not required for maintenance of the hypertension, which is related to the sustained increase in renal sympathetic nerve activity. As the air jet stress response is transduced by hypothalamic neurons, the authors speculate that this site is involved in the maintenance phase of the hypertension with a sustained increase in renal sympathetic nerve activity.The early effects of diet-induced fat accumulation on lumbar sympathetic nerve activity were also examined in rats over 15 days.2 Increases in brown and white adipose tissue (but not body weight) were accompanied by increases in plasma leptin (but not glucose) concentration and heart rate; however, mean a...

show abstract

Section: Selective Catheter-based Renal Sympathetic Denervationmentioning

confidence: 99%

Sympathetic Nervous System and Hypertension

2013

View full text Add to dashboard Cite

show abstract

“…Negative intrathoracic pressure and the autonomic nervous system In an animal model of OSA, negative tracheal pressure leads to a pronounced shortening of the atrial effective refractory period and increased atrial fibrillation inducibility, which are mediated by sympathetic a-and b-pathways, vagal activation and ganglionated plexus [56].…”

Section: Increased Negative Intrathoracic Pressurementioning

confidence: 99%

Effects of obstructive sleep apnoea on heart rhythm

2012

View full text Add to dashboard Cite

Symptomatic obstructive sleep apnoea (OSA) has been proven to be a risk factor for hypertension and vascular dysfunction, and has been proposed to be causally related with cardiac arrhythmias and sudden cardiac death.Searches of bibliographical databases revealed that several mechanisms seem to underpin the association between OSA and cardiac arrhythmias: intermittent hypoxia associated with autonomic nervous system activation and increased oxidative stress, which may lead to cardiac cellular damage and alteration in myocardial excitability; recurrent arousals, resulting in sympathetic activation and coronary vasoconstriction; and increased negative intrathoracic pressure which may mechanically stretch the myocardial walls and, thus, promote acute changes in myocardial excitability as well as structural remodelling of the myocardium.Findings from cross-sectional studies suggest a high prevalence of cardiac arrhythmias in patients with OSA and a high prevalence of OSA in those with cardiac arrhythmias. Preliminary evidence from uncontrolled interventional studies suggests that treatment of OSA may prevent cardiac arrhythmias.In conclusion, there is preliminary evidence that OSA is associated with the development of cardiac arrhythmias. Data from randomised controlled studies are needed to definitively clarify the role of OSA in arrhythmogenesis.

show abstract

“…Interestingly, NTP-induced atrial effective refractory period shortening was modulated by atropine or atenolol. In addition, the modulation of autonomic nervous system by renal sympathetic denervation displayed pronounced antiarrhythmic effects in the pig model for OSA (Linz et al 2012). These findings emphasize the importance of autonomic imbalance in OSA-associated AF.…”

mentioning

confidence: 59%