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Francois M. Abboud - One of the best experts on this subject based on the ideXlab platform.
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mechanisms determining sensitivity of Baroreceptor afferents in health and disease
Annals of the New York Academy of Sciences, 2006Co-Authors: Mark W. Chapleau, Silvana S Meyrelles, Francois M. AbboudAbstract:Baroreceptors sense and signal the central nervous system of changes in arterial pressure through a series of sensory processes. An increase in arterial pressure causes vascular distension and Baroreceptor deformation, the magnitude of which depends on the mechanical viscoelastic properties of the vessel wall. Classic methods (e.g., isolated carotid sinus preparation) and new approaches, including studies of isolated Baroreceptor neurons in culture, gene transfer using viral vectors, and genetically modified mice have been used to define the cellular and molecular mechanisms that determine Baroreceptor sensitivity. Deformation depolarizes the nerve endings by opening a new class of mechanosensitive Ion channel. This depolarization triggers action potential discharge through opening of voltage-dependent sodium (Na+) and potassium (K+) channels at the "spike initiating zone" (SIZ) near the sensory terminals. The resulting Baroreceptor activity and its sensitivity to changes in pressure are modulated through a variety of mechanisms that influence these sensory processes. Modulation of voltage-dependent Na+ and K+ channels and the Na+ pump at the SIZ by membrance potential, action potential discharge, and chemical autocrine and paracrine factors are important mechanisms contributing to changes in Baroreceptor sensitivity during sustained increases in arterial pressure and in pathological states associated with endothelial dysfunction, oxidative stress, and platelet activation.
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nitric oxide as an autocrine regulator of sodium currents in Baroreceptor neurons
Neuron, 1998Co-Authors: Mark W. Chapleau, James N Bates, Klaus Bielefeldt, Hon Chi Lee, Francois M. AbboudAbstract:Arterial Baroreceptors are mechanosensitive nerve endings in the aortic arch and carotid sinus that play a critical role in acute regulation of arterial blood pressure. A previous study has shown that nitric oxide (NO) or NO-related species suppress action potential discharge of Baroreceptors. In the present study, we investigated the effects of NO on Na+ currents of isolated Baroreceptor neurons in culture. Exogenous NO donors inhibited both tetrodotoxin (TTX) -sensitive and -insensitive Na+ currents. The inhibition was not mediated by cGMP but by NO interaction with channel thiols. Acute inhibition of NO synthase increased the Na+ currents. NO scavengers (hemoglobin and ferrous diethyldithiocarbamate) increased Na+ currents before but not after inhibition of NO synthase. Furthermore, NO production in the neuronal cultures was detected by chemiluminescence and immunoreactivity to the neuronal isoform of NO synthase was identified in fluorescently identified Baroreceptor neurons. These results indicate that NO/NO-related species function as autocrine regulators of Na+ currents in Baroreceptor neurons. Modulation of Na+ channels may represent a novel response to NO.
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Modulation of Baroreceptor Activity by Nitric Oxide and S-Nitrosocysteine
Circulation research, 1995Co-Authors: Tadashi Matsuda, James N Bates, Francois M. Abboud, Stephen J. Lewis, Mark W. ChapleauAbstract:Abstract The goal of this study was to determine whether nitric oxide (NO) and the NO donor, S -nitrosocysteine (cysNO), modulate the activity of carotid sinus Baroreceptors. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in anesthetized rabbits. Baroreceptor activity decreased in a dose-dependent manner after injection of either NO or cysNO as constant pressure was maintained, and activity recovered spontaneously over time, within seconds to minutes. The Baroreceptor pressure-activity relation was shifted significantly to the right by cysNO, with a profound suppression of activity at high pressure. Baroreceptor activity at 160 mm Hg averaged 76±8%, 60±6%, and 36±5% of the control maximum during exposure to 10−4, 2 to 3×10−4, and 10−3 mol/L cysNO, respectively. The inhibition of activity by the l and d isomers of cysNO was equivalent and was blocked by reduced hemoglobin, suggesting that the effect was mediated by NO. The suppression of Baroreceptor activity by cysNO was not related to vascular relaxation as measured by videomicrometer. Inhibition of soluble guanylate cyclase with methylene blue or 6-anilinoquinoline-5,8-quinone (LY83583, 10−5 mol/L) did not attenuate and dibutyryl cGMP (10−3 mol/L) did not mimic the suppression of Baroreceptor activity by cysNO, suggesting a cGMP-independent mechanism. Activation of endogenous NO formation with thimerosal (10−5 to 10−4 mol/L) reduced maximum Baroreceptor activity in five of eight experiments to 59±7% of the control maximum. The NO synthase inhibitor nitro-l-arginine methyl ester (L-NAME, 10−4 mol/L) by itself failed to influence Baroreceptor activity but prevented thimerosal-induced suppression of activity. Addition of l-arginine (10−3 mol/L) after L-NAME restored the inhibitory influence of thimerosal. The results indicate that NO and cysNO suppress Baroreceptor activity through a mechanism independent of guanylate cyclase activation and vascular relaxation and that endogenous NO released by chemical activation suppresses Baroreceptor activity.
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Modulation of Baroreceptor activity by ionic and paracrine mechanisms: an overview.
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 1994Co-Authors: Mark W. Chapleau, Francois M. AbboudAbstract:1. The primary mechanism of activation of Baroreceptors is mechanical deformation during vascular stretch. In addition, Baroreceptor activity is modulated by ionic mechanisms and by neurohumoral and paracrine factors that act directly on the nerve endings. 2. Ionic mechanisms play a major role in causing Baroreceptor activity to decline during a sustained increase in arterial pressure (adaptation) and in the suppression of activity that occurs after pressure returns to basal levels (post-excitatory depression). Activation of a 4-aminopyridine-sensitive K+ channel contributes to adaptation, whereas activation of an electrogenic sodium pump is responsible for post-excitatory depression. 3. Factors released from vascular endothelium exert powerful effects on Baroreceptor sensitivity. Prostacyclin increases Baroreceptor sensitivity and contributes to Baroreceptor activation during vascular stretch. Nitric oxide, endothelin and oxygen-derived free radicals suppress Baroreceptor activity particularly at high levels of arterial pressure. The sympathetic neurotransmitter norepinephrine modulates Baroreceptor activity: a) indirectly through its vasoconstrictor action, b) directly by binding to alpha-adrenergic receptors on the nerve endings, and c)through release of a cyclooxygenase metabolite, possibly prostacyclin, from endothelium. 4. Endothelial dysfunction contributes to Baroreceptor impairment in atherosclerosis and in chronic hypertension. Loss of the excitatory influence of prostacyclin and increased formation of free radicals and possibly endothelin contribute to the Baroreceptor dysfunction. Platelets aggregating at sites of endothelial damage in the carotid sinus release a stable diffusible factor that impairs Baroreceptor sensitivity. 5. Therapeutic interventions may alter Baroreceptor sensitivity through paracrine mechanisms. Treatment of hypertension or atherosclerosis may improve Baroreceptor sensitivity by restoring endothelial function. Antiplatelet agents may enhance Baroreceptor sensitivity. Antidepressant agents may decrease Baroreceptor sensitivity by inhibiting prostacyclin and/or stimulating nitric oxide formation, which may contribute to dysregulation of the circulation in patients treated for depression.
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Paracrine role of prostanoids in activation of arterial Baroreceptors: an overview.
Clinical and experimental hypertension. Part A Theory and practice, 1991Co-Authors: Mark W. Chapleau, G. Hajduczok, Francois M. AbboudAbstract:Baroreceptors located in carotid sinuses and aortic arch are activated with increases in arterial pressure. The increased afferent nerve activity triggers reflex adjustments that buffer the rise in pressure. Mechanical deformation of Baroreceptor nerve endings is considered the primary mechanism of receptor activation. Recent studies in our laboratory have demonstrated that prostanoids, most likely released from endothelial cells during stretch, contribute - as paracrine factors - to the activation of Baroreceptors. Exposure of the isolated carotid sinus in anesthetized rabbits to prostacyclin (PGI2) or arachidonic acid increases Baroreceptor sensitivity whereas inhibition of endogenous formation of prostanoids with indomethacin or aspirin decreases sensitivity. Baroreceptor sensitivity is also decreased after endothelial denudation and restored after adding PGI2 back to the denuded sinus suggesting that endothelium is the source of prostanoids that sensitize Baroreceptors. Pathologic states such as chron...
Mark W. Chapleau - One of the best experts on this subject based on the ideXlab platform.
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mechanisms determining sensitivity of Baroreceptor afferents in health and disease
Annals of the New York Academy of Sciences, 2006Co-Authors: Mark W. Chapleau, Silvana S Meyrelles, Francois M. AbboudAbstract:Baroreceptors sense and signal the central nervous system of changes in arterial pressure through a series of sensory processes. An increase in arterial pressure causes vascular distension and Baroreceptor deformation, the magnitude of which depends on the mechanical viscoelastic properties of the vessel wall. Classic methods (e.g., isolated carotid sinus preparation) and new approaches, including studies of isolated Baroreceptor neurons in culture, gene transfer using viral vectors, and genetically modified mice have been used to define the cellular and molecular mechanisms that determine Baroreceptor sensitivity. Deformation depolarizes the nerve endings by opening a new class of mechanosensitive Ion channel. This depolarization triggers action potential discharge through opening of voltage-dependent sodium (Na+) and potassium (K+) channels at the "spike initiating zone" (SIZ) near the sensory terminals. The resulting Baroreceptor activity and its sensitivity to changes in pressure are modulated through a variety of mechanisms that influence these sensory processes. Modulation of voltage-dependent Na+ and K+ channels and the Na+ pump at the SIZ by membrance potential, action potential discharge, and chemical autocrine and paracrine factors are important mechanisms contributing to changes in Baroreceptor sensitivity during sustained increases in arterial pressure and in pathological states associated with endothelial dysfunction, oxidative stress, and platelet activation.
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nitric oxide as an autocrine regulator of sodium currents in Baroreceptor neurons
Neuron, 1998Co-Authors: Mark W. Chapleau, James N Bates, Klaus Bielefeldt, Hon Chi Lee, Francois M. AbboudAbstract:Arterial Baroreceptors are mechanosensitive nerve endings in the aortic arch and carotid sinus that play a critical role in acute regulation of arterial blood pressure. A previous study has shown that nitric oxide (NO) or NO-related species suppress action potential discharge of Baroreceptors. In the present study, we investigated the effects of NO on Na+ currents of isolated Baroreceptor neurons in culture. Exogenous NO donors inhibited both tetrodotoxin (TTX) -sensitive and -insensitive Na+ currents. The inhibition was not mediated by cGMP but by NO interaction with channel thiols. Acute inhibition of NO synthase increased the Na+ currents. NO scavengers (hemoglobin and ferrous diethyldithiocarbamate) increased Na+ currents before but not after inhibition of NO synthase. Furthermore, NO production in the neuronal cultures was detected by chemiluminescence and immunoreactivity to the neuronal isoform of NO synthase was identified in fluorescently identified Baroreceptor neurons. These results indicate that NO/NO-related species function as autocrine regulators of Na+ currents in Baroreceptor neurons. Modulation of Na+ channels may represent a novel response to NO.
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Modulation of Baroreceptor Activity by Nitric Oxide and S-Nitrosocysteine
Circulation research, 1995Co-Authors: Tadashi Matsuda, James N Bates, Francois M. Abboud, Stephen J. Lewis, Mark W. ChapleauAbstract:Abstract The goal of this study was to determine whether nitric oxide (NO) and the NO donor, S -nitrosocysteine (cysNO), modulate the activity of carotid sinus Baroreceptors. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in anesthetized rabbits. Baroreceptor activity decreased in a dose-dependent manner after injection of either NO or cysNO as constant pressure was maintained, and activity recovered spontaneously over time, within seconds to minutes. The Baroreceptor pressure-activity relation was shifted significantly to the right by cysNO, with a profound suppression of activity at high pressure. Baroreceptor activity at 160 mm Hg averaged 76±8%, 60±6%, and 36±5% of the control maximum during exposure to 10−4, 2 to 3×10−4, and 10−3 mol/L cysNO, respectively. The inhibition of activity by the l and d isomers of cysNO was equivalent and was blocked by reduced hemoglobin, suggesting that the effect was mediated by NO. The suppression of Baroreceptor activity by cysNO was not related to vascular relaxation as measured by videomicrometer. Inhibition of soluble guanylate cyclase with methylene blue or 6-anilinoquinoline-5,8-quinone (LY83583, 10−5 mol/L) did not attenuate and dibutyryl cGMP (10−3 mol/L) did not mimic the suppression of Baroreceptor activity by cysNO, suggesting a cGMP-independent mechanism. Activation of endogenous NO formation with thimerosal (10−5 to 10−4 mol/L) reduced maximum Baroreceptor activity in five of eight experiments to 59±7% of the control maximum. The NO synthase inhibitor nitro-l-arginine methyl ester (L-NAME, 10−4 mol/L) by itself failed to influence Baroreceptor activity but prevented thimerosal-induced suppression of activity. Addition of l-arginine (10−3 mol/L) after L-NAME restored the inhibitory influence of thimerosal. The results indicate that NO and cysNO suppress Baroreceptor activity through a mechanism independent of guanylate cyclase activation and vascular relaxation and that endogenous NO released by chemical activation suppresses Baroreceptor activity.
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Modulation of Baroreceptor activity by ionic and paracrine mechanisms: an overview.
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 1994Co-Authors: Mark W. Chapleau, Francois M. AbboudAbstract:1. The primary mechanism of activation of Baroreceptors is mechanical deformation during vascular stretch. In addition, Baroreceptor activity is modulated by ionic mechanisms and by neurohumoral and paracrine factors that act directly on the nerve endings. 2. Ionic mechanisms play a major role in causing Baroreceptor activity to decline during a sustained increase in arterial pressure (adaptation) and in the suppression of activity that occurs after pressure returns to basal levels (post-excitatory depression). Activation of a 4-aminopyridine-sensitive K+ channel contributes to adaptation, whereas activation of an electrogenic sodium pump is responsible for post-excitatory depression. 3. Factors released from vascular endothelium exert powerful effects on Baroreceptor sensitivity. Prostacyclin increases Baroreceptor sensitivity and contributes to Baroreceptor activation during vascular stretch. Nitric oxide, endothelin and oxygen-derived free radicals suppress Baroreceptor activity particularly at high levels of arterial pressure. The sympathetic neurotransmitter norepinephrine modulates Baroreceptor activity: a) indirectly through its vasoconstrictor action, b) directly by binding to alpha-adrenergic receptors on the nerve endings, and c)through release of a cyclooxygenase metabolite, possibly prostacyclin, from endothelium. 4. Endothelial dysfunction contributes to Baroreceptor impairment in atherosclerosis and in chronic hypertension. Loss of the excitatory influence of prostacyclin and increased formation of free radicals and possibly endothelin contribute to the Baroreceptor dysfunction. Platelets aggregating at sites of endothelial damage in the carotid sinus release a stable diffusible factor that impairs Baroreceptor sensitivity. 5. Therapeutic interventions may alter Baroreceptor sensitivity through paracrine mechanisms. Treatment of hypertension or atherosclerosis may improve Baroreceptor sensitivity by restoring endothelial function. Antiplatelet agents may enhance Baroreceptor sensitivity. Antidepressant agents may decrease Baroreceptor sensitivity by inhibiting prostacyclin and/or stimulating nitric oxide formation, which may contribute to dysregulation of the circulation in patients treated for depression.
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Paracrine role of prostanoids in activation of arterial Baroreceptors: an overview.
Clinical and experimental hypertension. Part A Theory and practice, 1991Co-Authors: Mark W. Chapleau, G. Hajduczok, Francois M. AbboudAbstract:Baroreceptors located in carotid sinuses and aortic arch are activated with increases in arterial pressure. The increased afferent nerve activity triggers reflex adjustments that buffer the rise in pressure. Mechanical deformation of Baroreceptor nerve endings is considered the primary mechanism of receptor activation. Recent studies in our laboratory have demonstrated that prostanoids, most likely released from endothelial cells during stretch, contribute - as paracrine factors - to the activation of Baroreceptors. Exposure of the isolated carotid sinus in anesthetized rabbits to prostacyclin (PGI2) or arachidonic acid increases Baroreceptor sensitivity whereas inhibition of endogenous formation of prostanoids with indomethacin or aspirin decreases sensitivity. Baroreceptor sensitivity is also decreased after endothelial denudation and restored after adding PGI2 back to the denuded sinus suggesting that endothelium is the source of prostanoids that sensitize Baroreceptors. Pathologic states such as chron...
Harald Rau - One of the best experts on this subject based on the ideXlab platform.
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Effects of Baroreceptor stimulation and opioids on the auditory startle reflex
Psychophysiology, 2005Co-Authors: Ivan Nyklíček, V.j.m. Wijnen, Harald RauAbstract:We examined (a) whether carotid Baroreceptor stimulation attenuates the auditory startle response and its modulation by preceding affective pictures, and (b) whether these effects are mediated by endogenous opioids. Seventy-eight young normotensive adults with or without a parental history of hypertension received brief exposures to affective pictures and noise bursts during phasic manipulation of the carotid Baroreceptors. In each participant, opioids were blocked by naltrexone in half of the sessions. Baroreceptor stimulation had a strong dampening effect on the startle response. This effect was not influenced by opioid blockade, sex, or parental history of hypertension. No Baroreceptor effects were obtained regarding ratings of the affective pictures or startle modulation by the pictures. The Baroreceptor stimulation effects seem to be mediated by the basal primary acoustic startle circuit rather than by higher affective circuits.
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pres and orthostatic induced heart rate changes as markers of labile hypertension magnitude and reliability measures
Biological Psychology, 1996Co-Authors: Harald Rau, John J Furedy, Thomas ElbertAbstract:Abstract Split-half and test-retest reliabilities of heart-rate responses to a Baroreceptor manipulation and an orthostatic maneuver were compared between subjects with either normal or elevated blood-pressure. Ten subjects showing elevated resting blood-pressure and 11 normotensive subjects participated in two experimental sessions, each including heart-rate recordings during Baroreceptor manipulation and orthostatic challenge. Carotid Baroreceptors were manipulated by applying the Baroreceptor-specific phase-related external suction (PRES) technique. The orthostatic stimulation procedure (OSP) was a change of body position from lying to standing. Heart rate responses evoked by OSP failed to discriminate significantly between the groups either in the magnitude or the (test/retest) reliability measure. The PRES procedure also failed to discriminate with the conventional magnitude measure, but the reliability measures showed significant differences. Paradoxically, the high-blood-pressure group manifested the higher Baroreceptor reliability. The present findings are consistent with the view that operant conditioning produces phasic blood-pressure increases. In this view, blood-pressure increases activate the arterial Baroreceptors which, in turn, dampen pain and/or stress sensitivity. Individuals showing high consistency (reliability) in their cardiovascular responses are more likely to learn this form of conditioning, and hence to eventually increase their tonic blood-pressure. High reliability of cardiovascular responses may therefore constitute a risk for hypertension. Aside from such theoretical considerations, the findings indicate that less conventional dependent variables like reliability may be worth exploring in the search for the etiology of essential hypertension, and that, in this search, specificity (relative to Baroreceptor function) is more important than the magnitude of the heart-rate changes that are produced.
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Baroreceptor cortical effects, emotions and pain
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 1995Co-Authors: Alessio Mini, Harald Rau, Pedro Montoya, Daniela Palomba, Niels BirbaumerAbstract:Abstract The specificity of Baroreceptor-dependent inhibition of pain reactions to electrical stimuli was investigated during induction of different emotional states in 27 subjects. Baroreceptors were stimulated through the PRES (Phase Related External Suction) technique, while emotions were induced by means of pleasant, neutral and unpleasant slides. The dependent variables were pain ratings, somatic evoked potentials (N150 and P260) recorded from Fz, Cz and Pz, and skin conductance response (SCR), while heart rate was recorded as a PRES requirement. Valence and arousal ratings were obtained in front of each slide. During suction (external Baroreceptor activation) reduced pain ratings, cortical disfacilitation (from Pz, as revealed by N150) and lower SCR were found as compared to pressure (Baroreceptor deactivation). Moreover, brain evoked potentials (N150 and P260) reflecting cortical inhibition were found under condition of Baroreceptor stimulation during unpleasant slides, but not during pleasant or neutral ones: this result was found in the high blood pressure subjects only. Data showed also a valence effect on pain ratings: pain was evaluated to be higher during unpleasant slides, than neutral and pleasant ones. Results are discussed in the light of “Baroreceptor reward” hypothesis, which proposes a learning mechanism for the development of essential hypertension.
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central effects of Baroreceptor activation in humans attenuation of skeletal reflexes and pain perception
Proceedings of the National Academy of Sciences of the United States of America, 1994Co-Authors: Barry R Dworkin, Harald Rau, Thomas Elbert, Paul Pauli, Niels Birbaumer, Conrad Droste, C H M BruniaAbstract:Abstract Activating the arterial Baroreceptors blunts pain sensation and produces other forms of central nervous system inhibition in animals. These effects may be important to blood pressure regulation but have not been rigorously verified in humans. We describe (i) a noninvasive behaviorally unbiased method for Baroreceptor stimulation and (ii) the application of this method to measurement of Baroreceptor-mediated attenuation of pain perception and of the Achilles tendon reflex. The findings are relevant to basic mechanisms of blood pressure stabilization and cardiovascular reactivity and may also have implications for noncompliance with antihypertensive medications and for the pathophysiology of essential hypertension.
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Activation of carotid Baroreceptors inhibits spinal reflexes in man
Electroencephalography and clinical neurophysiology, 1993Co-Authors: Harald Rau, Stuart Brody, Cornelis H. M. Brunia, E. P. J. Damen, Thomas ElbertAbstract:Abstract The present study was designed to investigate the effect of Baroreceptors on a spinal reflex. The Achilles tendon reflex (T reflex), a monosynaptic spinal reflex, was chosen as an indicator of descending influences of central activation. The Baroreceptors are stretch receptors which respond to extensions of the arterial wall. Carotid sinus Baroreceptors can be manipulated non-invasively by means of a cuff around the neck. In this study, the phase-related external suction (PRES) neck cuff technique was used. PRES applies short changes in cuff pressure as a function of heart cycle phase, controlling for non-specific effects found in other Baroreceptor manipulation methods. The T reflex was reduced when elicited during the highest levels of Baroreceptor activation. Reflex amplitude was largest when elicited during the lowest levels of Baroreceptor activation. These results are consistent with previous findings that Baroreceptor activation reduces CNS excitability.
William Maixner - One of the best experts on this subject based on the ideXlab platform.
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Baroreceptor modulation of the cardiovascular system pain consciousness and cognition
Comprehensive Physiology, 2021Co-Authors: Heberto Suarezroca, Negmeldeen F Mamoun, Martin I Sigurdson, William MaixnerAbstract:Baroreceptors are mechanosensitive elements of the peripheral nervous system that maintain cardiovascular homeostasis by coordinating the responses to external and internal environmental stressors. While it is well known that carotid and cardiopulmonary Baroreceptors modulate sympathetic vasomotor and parasympathetic cardiac neural autonomic drive, to avoid excessive fluctuations in vascular tone and maintain intravascular volume, there is increasing recognition that Baroreceptors also modulate a wide range of non-cardiovascular physiological responses via projections from the nucleus of the solitary tract to regions of the central nervous system, including the spinal cord. These projections regulate pain perception, sleep, consciousness, and cognition. In this article, we summarize the physiology of Baroreceptor pathways and responses to Baroreceptor activation with an emphasis on the mechanisms influencing cardiovascular function, pain perception, consciousness, and cognition. Understanding Baroreceptor-mediated effects on cardiac and extra-cardiac autonomic activities will further our understanding of the pathophysiology of multiple common clinical conditions, such as chronic pain, disorders of consciousness (e.g., abnormalities in sleep-wake), and cognitive impairment, which may result in the identification and implementation of novel treatment modalities. © 2021 American Physiological Society. Compr Physiol 11:1373-1423, 2021.
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Contribution of Baroreceptor Function to Pain Perception and Perioperative Outcomes.
Anesthesiology, 2019Co-Authors: Heberto Suarez-roca, Rebecca Y. Klinger, Mihai V. Podgoreanu, Martin I. Sigurdsson, Nathan H. Waldron, Joseph P. Mathew, William MaixnerAbstract:Baroreceptors are mechanosensitive elements of the peripheral nervous system that maintain homeostasis by coordinating physiologic responses to external and internal stimuli. While it is recognized that carotid and cardiopulmonary Baroreceptor reflexes modulate autonomic output to mitigate excessive fluctuations in arterial blood pressure and to maintain intravascular volume, increasing evidence suggests that baroreflex pathways also project to key regions of the central nervous system that regulate somatosensory, somatomotor, and central nervous system arousal. In addition to maintaining autonomic homeostasis, Baroreceptor activity modulates the perception of pain, as well as neuroimmune, neuroendocrine, and cognitive responses to physical and psychologic stressors. This review summarizes the role that Baroreceptor pathways play in modulating acute and chronic pain perception. The contribution of Baroreceptor function to postoperative outcomes is also presented. Finally, methods that enhance Baroreceptor function, which hold promise in improving postoperative and pain management outcomes, are presented.
Julian F. R. Paton - One of the best experts on this subject based on the ideXlab platform.
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heartbeats entrain breathing via Baroreceptor mediated modulation of expiratory activity
Experimental Physiology, 2021Co-Authors: William H Barnett, Julian F. R. Paton, David M Baekey, Thomas E Dick, Erica A Wehrwein, Yaroslav I MolkovAbstract:New findings Cardio-ventilatory coupling refers to the onset of inspiration occurring at a preferential latency following the last heartbeat in expiration. According to the cardiac-trigger hypothesis, the pulse pressure initiates an inspiration via Baroreceptor activation. However, the central neural substrate mediating this coupling remains undefined. Using a combination of animal data, human data and mathematical modeling, this study tests the hypothesis that the heartbeat, by way of pulsatile baroreflex activation, controls the initiation of inspiration which occurs through a rapid neural activation loop from the carotid Baroreceptors to Botzinger Complex expiratory neurons. Abstract Cardio-ventilatory coupling refers to a heartbeat (HB) occurring at a preferred latency prior to the next breath. We hypothesized that the pressure pulse generated by a HB activates Baroreceptors that modulates brainstem expiratory neuronal activity and delays the initiation of inspiration. In supine male subjects, we recorded ventilation, electrocardiogram, and blood pressure during 20-min epochs of baseline, slow-deep breathing, and recovery. In in situ rodent preparations, we recorded brainstem activity in response to pulses of perfusion pressure. We applied a well-established respiratory network model to interpret these data. In humans, the latency between a HB and onset of inspiration was consistent across different breathing patterns. In in situ preparations, a transient pressure pulse during expiration activated a subpopulation of expiratory neurons normally active during post-inspiration; thus, delaying the next inspiration. In the model, Baroreceptor input to post-inspiratory neurons accounted for the effect. These studies are consistent with baroreflex activation modulating respiration through a pauci-synaptic circuit from Baroreceptors to onset of inspiration. This article is protected by copyright. All rights reserved.
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effect of Baroreceptor stimulation on the respiratory pattern insights into respiratory sympathetic interactions
Respiratory Physiology & Neurobiology, 2010Co-Authors: David M Baekey, Julian F. R. Paton, Ilya A. Rybak, Yaroslav I Molkov, Thomas E DickAbstract:Sympathetic nerve activity (SNA) is modulated by respiratory activity which indicates the existence of direct interactions between the respiratory and sympathetic networks within the brainstem. Our experimental studies reveal that Te prolongation evoked by Baroreceptor stimulation varies with respiratory phase and depends on the pons. We speculate that the sympathetic Baroreceptor reflex, providing negative feedback from Baroreceptors to the rostral ventrolateral medulla and SNA, has two pathways: one direct and independent of the respiratory–sympathetic interactions and the other operating via the respiratory pattern generator and is hence dependent on the respiratory modulation of SNA. Our experimental studies in the perfused in situ rat preparation and complementary computational modelling studies support the hypothesis that Baroreceptor activation during expiration prolongs the Te via transient activation of post-inspiratory and inhibition of augmenting expiratory neurones of the Botzinger Complex (BotC). We propose that these BotC neurones are also involved in the respiratory modulation of SNA, and contribute to the respiratory modulation of the sympathetic Baroreceptor reflex. © 2010 Elsevier B.V. All rights reserved.
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Baroreflex inhibition of cardiac sympathetic outflow is attenuated by angiotensin II in the nucleus of the solitary tract
Neuroscience, 2001Co-Authors: Pedro Boscan, Andrew M Allen, Julian F. R. PatonAbstract:Homeostatic regulation of arterial pressure is maintained by arterial Baroreceptors. Activation of these receptors results in an inhibition of sympathetic activity to the heart. It is known that angiotensin II in the nucleus tractus solitarii attenuates the Baroreceptor reflex-evoked vagal bradycardia. Here, we determined whether the cardiac sympathetic component of the Baroreceptor reflex could be modulated by angiotensin II in the nucleus of the solitary tract. An in situ, arterially perfused working heart–brainstem preparation of rat was employed and the sympathetic inferior cardiac nerve recorded. Increases in perfusion pressure caused a reflex bradycardia and inhibition of inferior cardiac nerve activity. Microinjection of angiotensin II (500 fmol) in the nucleus of the solitary tract attenuated significantly both the reflex bradycardia and inhibition of inferior cardiac nerve activity (P