Chemoreceptor Reflex

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Julian F R Paton - One of the best experts on this subject based on the ideXlab platform.

  • ISH NIA OS-04 P2X3 RECEPTOR ACTIVITY IN THE CAROTID BODY (CB) OF SPONTANEOUSLY HYPERTENSIVE (SH) RATS CONTRIBUTES TO INCREASED CHEMOReflex HYPERSENSITIVITY AND HYPERTENSION
    Journal of Hypertension, 2016
    Co-Authors: Wioletta Pijacka, Fiona D. Mcbryde, Anthony P. D. W. Ford, Julian F R Paton
    Abstract:

    Objective:Arterial hypertension is associated with increases in both peripheral Chemoreceptor Reflex sensitivity and sympathetic nerve activity (SNA). We have shown that CB resection in SH rats reduces arterial pressure (AP; McBryde et al. 2013). Since P2X3 receptors exist in the rat CB and P2X3 rec

  • ReflexLY EVOKED COACTIVATION OF CARDIAC VAGAL AND SYMPATHETIC MOTOR OUTFLOWS: OBSERVATIONS AND FUNCTIONAL IMPLICATIONS
    Clinical and Experimental Pharmacology and Physiology, 2006
    Co-Authors: Julian F R Paton, Pedro Boscan, Eugene Nalivaiko, Anthony E Pickering
    Abstract:

    1. The purpose of the present review is to highlight the pattern of activity in the parasympathetic and sympathetic nerves innervating the heart during their Reflex activation. 2. We describe the well-known reciprocal control of cardiac vagal and sympathetic activity during the baroreceptor Reflex, but point out that this appears to be the exception rather than the rule and that many other Reflexes reviewed herein (e.g. peripheral Chemoreceptor, nociceptor, diving response and oculocardiac) involve simultaneous coactivation of both autonomic limbs. 3. The heart rate response during simultaneous activation of cardiac autonomic outflows is unpredictable because it does not simply reflect the summation of opposing influences. Indeed, it can result in bradycardia (peripheral Chemoreceptor, diving and corneal), tachycardia (nociceptor) and, in some circumstances, can predispose to malignant arrhythmias. 4. We propose that this cardiac autonomic coactivation may allow greater cardiac output during bradycardia (increased ventricular filling time and stronger contraction) than activation of the sympathetic limb alone. This may be important when pumping blood into a constricted vascular tree, such as is the case during the peripheral Chemoreceptor Reflex and the diving response.

  • Sensory afferent selective role of P2 receptors in the nucleus tractus solitarii for mediating the cardiac component of the peripheral Chemoreceptor Reflex in rats.
    The Journal of physiology, 2002
    Co-Authors: Julian F R Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H. Machado, Pedro Boscan
    Abstract:

    We have assessed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissural nucleus tractus solitarii (NTS) in mediating the peripheral Chemoreceptor Reflex cardiorespiratory response in the arterially perfused in situ working heart-brainstem preparation of rats. Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2',4'-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the Reflex bradycardia (by approximately 50 %), but not the tachypnoea, following peripheral Chemoreceptor stimulation. In contrast, the Reflex bradycardia produced by stimulation of pharyngo-oesophageal receptors was unaffected. Furthermore, microinjections in NTS of the P2X receptor agonist alpha,beta-methyleneadenosine 5'-triphosphate (10 pmol) evoked a bradycardia which was antagonized by suramin (100 pmol). This P2X agonist reversibly potentiated the peripheral Chemoreceptor-evoked bradycardia. The effect of suramin was selective to purinergic receptors because the bradycardia evoked by microinjection of alpha,beta-methyleneadenosine 5'-triphosphate was blocked while the bradycardic responses to microinjections of NMDA or non-NMDA receptor agonists were not affected. From whole-cell recordings, some NTS neurones received convergent excitatory synaptic inputs from both peripheral Chemoreceptors and receptors at the pharyngo-oesophageal junction. The excitatory postsynaptic response evoked by Chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-oesophageal receptors were unperturbed. Our findings support the hypothesis that caudal commissural NTS P2 purinergic receptors play a role in the neurotransmission of the parasympathetic (bradycardic) component of the Chemoreceptor Reflex. This effect is highly selective in that the Chemoreceptor afferent-evoked tachypnoea, as well as other visceral receptor-mediated Reflex bradycardia, remain unaffected.

  • Sensory Afferent Selective Role of P2 Receptors in the Nucleus Tractus Solitarii for Mediating the Cardiac Component of the Peripheral Chemoreceptor Reflex in Rats
    The Journal of Physiology, 2002
    Co-Authors: Julian F R Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H. Machado, Pedro Boscan
    Abstract:

    We have assessed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissural nucleus tractus solitarii (NTS) in mediating the peripheral Chemoreceptor Reflex cardiorespiratory response in the arterially perfused in situ working heart-brainstem preparation of rats. Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2′,4′-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the Reflex bradycardia (by ≈50 %), but not the tachypnoea, following peripheral Chemoreceptor stimulation. In contrast, the Reflex bradycardia produced by stimulation of pharyngo-oesophageal receptors was unaffected. Furthermore, microinjections in NTS of the P2X receptor agonist α,β-methyleneadenosine 5′-triphosphate (10 pmol) evoked a bradycardia which was antagonized by suramin (100 pmol). This P2X agonist reversibly potentiated the peripheral Chemoreceptor-evoked bradycardia. The effect of suramin was selective to purinergic receptors because the bradycardia evoked by microinjection of α,β-methyleneadenosine 5′-triphosphate was blocked while the bradycardic responses to microinjections of NMDA or non-NMDA receptor agonists were not affected. From whole-cell recordings, some NTS neurones received convergent excitatory synaptic inputs from both peripheral Chemoreceptors and receptors at the pharyngo-oesophageal junction. The excitatory postsynaptic response evoked by Chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-oesophageal receptors were unperturbed. Our findings support the hypothesis that caudal commissural NTS P2 purinergic receptors play a role in the neurotransmission of the parasympathetic (bradycardic) component of the Chemoreceptor Reflex. This effect is highly selective in that the Chemoreceptor afferent-evoked tachypnoea, as well as other visceral receptor-mediated Reflex bradycardia, remain unaffected.

  • Nociceptive afferents selectively modulate the cardiac component of the peripheral Chemoreceptor Reflex via actions within the solitary tract nucleus
    Neuroscience, 2002
    Co-Authors: P Boscan, Julian F R Paton
    Abstract:

    Abstract Our previous findings showed that the nucleus of the solitary tract (NTS) mediated part of the tachycardia evoked during somatic noxious stimulation. Here, we investigated the interaction between somatic nociceptor- and peripheral Chemoreceptor-evoked cardiac changes. We sought to determine whether this interaction occurred within the NTS, the primary site of termination of Chemoreceptor afferents. In a working heart–brainstem preparation of rat, mechanical noxious activation of a forelimb evoked a tachycardia of 17.5±3 (mean±S.E.M.) b.p.m., whereas sodium cyanide (7–30 μg) stimulation of peripheral Chemoreceptors produced a sub-maximal bradycardia of −140±15 b.p.m. During nociceptor stimulation the sodium cyanide-evoked bradycardia was attenuated to −42.6±12 b.p.m. but could be prevented by a multiple bilateral NTS microinjection of bicuculline (i.e. −173±18 b.p.m.). Furthermore, the activity of NTS neurones responding to peripheral Chemoreceptor stimulation increased from 2.8±1.3 to 9.4±1.9 Hz during sodium cyanide injection ( n =7; P We conclude that somatic noxious stimulation attenuates the Chemoreceptor Reflex-evoked bradycardia via a GABA A ergic mechanism in the NTS.

Masahiko Suzuki - One of the best experts on this subject based on the ideXlab platform.

  • benzodiazepine sensitive gabaa receptors in the commissural subnucleus of the nts are involved in the carotid Chemoreceptor Reflex in rats
    Autonomic Neuroscience: Basic and Clinical, 2004
    Co-Authors: Masahiko Suzuki, Masami Nishina, Shinichi Nakamura, Kei Maruyama
    Abstract:

    Abstract We studied the role of benzodiazepine (BDZ) receptors in the commissural subnucleus of the nucleus tractus solitarius (commNTS) in Chemoreceptor Reflex in urethane-anesthetized, pancronium-immobilized, artificially ventilated and bilaterally vagotomized rats. A BDZ agonist, diazepam (1–4 μmol/kg), administered intravenously reduced resting phrenic nerve activity (PNA) and blood pressure (BP). Stimulation of carotid Chemoreceptors induced an increase in PNA and an increase in BP. Diazepam inhibited this Chemoreceptor Reflex. The effects of intravenous injection of diazepam (4 μmol/kg) on the Chemoreceptor Reflex were antagonized by microinjection of the BDZ antagonist flumazenil (100 pmol) into the commNTS. Microinjection of flumazenil (100 pmol) alone had no effect on the basal PNA and BP, and the Chemoreceptor Reflex. These results suggest that BDZ receptors are present in the carotid Chemoreceptor Reflex pathway in the commNTS and potentiate GABA A transmission.

  • endogenous gaba in the commissural subnucleus of the nts inhibits the carotid Chemoreceptor Reflex via gaba a receptors in rats
    Journal of Neural Transmission, 2003
    Co-Authors: Masahiko Suzuki, Masami Nishina, Shinichi Nakamura, Kei Maruyama
    Abstract:

    Using urethane-chloralose anesthetized rats, we investigated which GABA receptor is responsible for the action of endogenous GABA on the carotid Chemoreceptor Reflex in the commissural subnucleus of the nucleus tractus solitarius (commNTS). Microinjection of the selective GABA uptake inhibitor nipecotic acid (40 nmol) into the commNTS attenuated the increases in respiration (respiratory movement and rate) and the elevation in arterial blood pressure elicited by carotid Chemoreceptor stimulation. These effects were completely antagonized by premicroinjection of the GABAA antagonist bicuculline (20 pmol), but not of the GABAB antagonist 2-OH-saclofen (400 pmol), into the same site. These findings suggest that endogenous GABA mainly acts on GABAA receptors, and inhibits the Chemoreceptor Reflex in the commNTS in rats.

  • gabab receptors in the nucleus tractus solitarii modulate the carotid Chemoreceptor Reflex in rats
    Neuroscience Letters, 1999
    Co-Authors: Masahiko Suzuki, Mitsue Tetsuka, Makoto Endo
    Abstract:

    Abstract In urethane-chloralose anesthetized rats, the role of GABA B receptor in the commissural subnucleus of the nucleus tractus solitarii (commNTS) on the carotid Chemoreceptor Reflex was investigated. Microinjection of a GABA B agonist baclofen into the commNTS did not have any effects on arterial blood pressure (BP) or respiration (RP), while it attenuated the increases in BP and RP elicited by carotid Chemoreceptor stimulation. These effects were blocked by microinjection of a GABA B antagonist 2-OH-saclofen into the same site. Prior microinjection of 2-OH-saclofen did not have any effects on the chemoReflex or on resting BP or RP, while the effects of baclofen on the chemoReflex were completely blocked. These results suggest that GABA B receptors are present in the carotid Chemoreceptor Reflex pathway in commNTS and modulate the Chemoreceptor Reflex.

Virend K. Somers - One of the best experts on this subject based on the ideXlab platform.

  • Sleep Apnea, Hypertension and the Sympathetic Nervous System in the Adult Population.
    Journal of Clinical Medicine, 2020
    Co-Authors: Shreyas Venkataraman, Soumya Vungarala, Naima Covassin, Virend K. Somers
    Abstract:

    Sleep apnea is very common in patients with cardiovascular disease, especially in patients with hypertension. Over the last few decades a number of discoveries have helped support a causal relationship between the two and even resistant hypertension. The role neurogenic mechanisms play has gathered more attention in the recent past due to their immediate bedside utility. Several innovative discoveries in pathogenesis including those exploring the role of baroReflex gain, cardiovascular variability, Chemoreceptor Reflex activation and the sympathetic nervous system have emerged. In this review, we discuss the epidemiology of sleep apnea and hypertension and the pathogenic mechanisms contributing to neurogenic hypertension. Furthermore, recent management strategies in addition to continuous positive airway pressure (CPAP), such as upper airway stimulation and renal denervation that target these pathogenic mechanisms, are also discussed.

  • interaction of baroreceptor and Chemoreceptor Reflex control of sympathetic nerve activity in normal humans
    Journal of Clinical Investigation, 1991
    Co-Authors: Virend K. Somers, A L Mark, Francois M Abboud
    Abstract:

    : Animal studies have demonstrated that activation of the baroReflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral Chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroReflex activation on the sympathetic response to stimulation of PC and central Chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central Chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal Reflex control to determine the selectivity of the interactive influence of baroReflex activation. BaroReflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 +/- 92 to 354 +/- 107 U/min (P less than 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05). With hypoxia during baroReflex activation with PE, SNA did not increase (50 +/- 23 U/min). During hypercapnia alone, SNA increased from 116 +/- 39 to 234 +/- 72 U/min (P less than 0.01). Hypercapnia during baroReflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroReflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroReflex and the peripheral chemoReflex may be explained by convergence of baroreceptor and peripheral Chemoreceptor afferents on neurons in the medulla.

Ramon Alvarezbuylla - One of the best experts on this subject based on the ideXlab platform.

  • carotid Chemoreceptor Reflex modulation by arginine vasopressin microinjected into the nucleus tractus solitarius in rats
    Archives of Medical Research, 2006
    Co-Authors: Sergio Montero, Alexander Yarkov, Monica Lemus, Elena Roces De Alvarezbuylla, Ramon Alvarezbuylla
    Abstract:

    Background In addition to their role of sensing O 2 , pH, CO 2 , osmolarity and temperature, carotid body receptors (CBR) were proposed by us and others to have a glucose-sensing role in the blood entering the brain, integrating information about blood glucose and O 2 levels essential for central nervous system (CNS) metabolism. The nucleus tractus solitarius (NTS) is an important relay station in central metabolic control and receives signals from peripheral glucose-sensitive hepatoportal afferences, from central glucose-responsive neurons in the brainstem and from CBR and arginine–vasopressin (AVP)-containing axons from hypothalamic nuclei. Methods In normal Wistar rats anesthetized with pentobarbital, permanent cannulas were placed stereotaxically in the NTS. Glucose changes were induced in vivo after CBR stimulation with sodium cyanide (NaCN-5 μg/100 g), preceded by an infusion of AVP [(10 or 40 pmol/100 nL of artificial cerebrospinal fluid) aCSF] or an antagonist for V1a receptors (anti-glycogenolytic vasopressin analogue-VP1-A) (100 pmol/100 nL of aCSF) into the NTS. Results CBR stimulation after an AVP infusion (larger dose) into the NTS resulted in a significantly higher arterial glucose and lower brain arterial–venous glucose difference. In the same way, VP1-A administration in the NTS significantly decreased the effects observed after AVP priming before CBR stimulation or preceding the CBR stimulation, alone. Conclusions We propose that AVP in the NTS could participate in glucose homeostasis, modulating the information arising in CBR after histotoxic-anoxia stimulation.

Pedro Boscan - One of the best experts on this subject based on the ideXlab platform.

  • ReflexLY EVOKED COACTIVATION OF CARDIAC VAGAL AND SYMPATHETIC MOTOR OUTFLOWS: OBSERVATIONS AND FUNCTIONAL IMPLICATIONS
    Clinical and Experimental Pharmacology and Physiology, 2006
    Co-Authors: Julian F R Paton, Pedro Boscan, Eugene Nalivaiko, Anthony E Pickering
    Abstract:

    1. The purpose of the present review is to highlight the pattern of activity in the parasympathetic and sympathetic nerves innervating the heart during their Reflex activation. 2. We describe the well-known reciprocal control of cardiac vagal and sympathetic activity during the baroreceptor Reflex, but point out that this appears to be the exception rather than the rule and that many other Reflexes reviewed herein (e.g. peripheral Chemoreceptor, nociceptor, diving response and oculocardiac) involve simultaneous coactivation of both autonomic limbs. 3. The heart rate response during simultaneous activation of cardiac autonomic outflows is unpredictable because it does not simply reflect the summation of opposing influences. Indeed, it can result in bradycardia (peripheral Chemoreceptor, diving and corneal), tachycardia (nociceptor) and, in some circumstances, can predispose to malignant arrhythmias. 4. We propose that this cardiac autonomic coactivation may allow greater cardiac output during bradycardia (increased ventricular filling time and stronger contraction) than activation of the sympathetic limb alone. This may be important when pumping blood into a constricted vascular tree, such as is the case during the peripheral Chemoreceptor Reflex and the diving response.

  • Sensory afferent selective role of P2 receptors in the nucleus tractus solitarii for mediating the cardiac component of the peripheral Chemoreceptor Reflex in rats.
    The Journal of physiology, 2002
    Co-Authors: Julian F R Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H. Machado, Pedro Boscan
    Abstract:

    We have assessed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissural nucleus tractus solitarii (NTS) in mediating the peripheral Chemoreceptor Reflex cardiorespiratory response in the arterially perfused in situ working heart-brainstem preparation of rats. Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2',4'-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the Reflex bradycardia (by approximately 50 %), but not the tachypnoea, following peripheral Chemoreceptor stimulation. In contrast, the Reflex bradycardia produced by stimulation of pharyngo-oesophageal receptors was unaffected. Furthermore, microinjections in NTS of the P2X receptor agonist alpha,beta-methyleneadenosine 5'-triphosphate (10 pmol) evoked a bradycardia which was antagonized by suramin (100 pmol). This P2X agonist reversibly potentiated the peripheral Chemoreceptor-evoked bradycardia. The effect of suramin was selective to purinergic receptors because the bradycardia evoked by microinjection of alpha,beta-methyleneadenosine 5'-triphosphate was blocked while the bradycardic responses to microinjections of NMDA or non-NMDA receptor agonists were not affected. From whole-cell recordings, some NTS neurones received convergent excitatory synaptic inputs from both peripheral Chemoreceptors and receptors at the pharyngo-oesophageal junction. The excitatory postsynaptic response evoked by Chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-oesophageal receptors were unperturbed. Our findings support the hypothesis that caudal commissural NTS P2 purinergic receptors play a role in the neurotransmission of the parasympathetic (bradycardic) component of the Chemoreceptor Reflex. This effect is highly selective in that the Chemoreceptor afferent-evoked tachypnoea, as well as other visceral receptor-mediated Reflex bradycardia, remain unaffected.

  • Sensory Afferent Selective Role of P2 Receptors in the Nucleus Tractus Solitarii for Mediating the Cardiac Component of the Peripheral Chemoreceptor Reflex in Rats
    The Journal of Physiology, 2002
    Co-Authors: Julian F R Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H. Machado, Pedro Boscan
    Abstract:

    We have assessed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissural nucleus tractus solitarii (NTS) in mediating the peripheral Chemoreceptor Reflex cardiorespiratory response in the arterially perfused in situ working heart-brainstem preparation of rats. Microinjection in NTS of either suramin (100 pmol) or pyrinoxalphosphate-6-azophenyl-2′,4′-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the Reflex bradycardia (by ≈50 %), but not the tachypnoea, following peripheral Chemoreceptor stimulation. In contrast, the Reflex bradycardia produced by stimulation of pharyngo-oesophageal receptors was unaffected. Furthermore, microinjections in NTS of the P2X receptor agonist α,β-methyleneadenosine 5′-triphosphate (10 pmol) evoked a bradycardia which was antagonized by suramin (100 pmol). This P2X agonist reversibly potentiated the peripheral Chemoreceptor-evoked bradycardia. The effect of suramin was selective to purinergic receptors because the bradycardia evoked by microinjection of α,β-methyleneadenosine 5′-triphosphate was blocked while the bradycardic responses to microinjections of NMDA or non-NMDA receptor agonists were not affected. From whole-cell recordings, some NTS neurones received convergent excitatory synaptic inputs from both peripheral Chemoreceptors and receptors at the pharyngo-oesophageal junction. The excitatory postsynaptic response evoked by Chemoreceptor stimulation was depressed by suramin, but convergent excitatory inputs from pharyngo-oesophageal receptors were unperturbed. Our findings support the hypothesis that caudal commissural NTS P2 purinergic receptors play a role in the neurotransmission of the parasympathetic (bradycardic) component of the Chemoreceptor Reflex. This effect is highly selective in that the Chemoreceptor afferent-evoked tachypnoea, as well as other visceral receptor-mediated Reflex bradycardia, remain unaffected.

  • the nucleus of the solitary tract an integrating station for nociceptive and cardiorespiratory afferents
    Experimental Physiology, 2002
    Co-Authors: Pedro Boscan, Anthony E Pickering, Julian F R Paton
    Abstract:

    Painful stimuli can evoke dramatic responses in the cardiovascular and respiratory systems. We have assessed the role of both the sympathetic and parasympathetic nervous system in mediating the Reflex tachycardia that accompanies somatic nociception. We describe a major role for the nucleus tractus solitarii (NTS) as a site for integrating nociceptive and cardiorespiratory afferents. Since cardiorespiratory and nociceptive afferents terminate in the NTS, this nucleus offers a powerful opportunity for central modulation. We show that the NTS plays a major role in mediating the Reflex tachycardia evoked by somatic noxious stimulation. Similar noxious stimulation attenuates the cardiac component of the peripheral Chemoreceptor Reflex and inhibits the peripheral Chemoreceptor-evoked excitatory synaptic response of some NTS neurones. The functional interpretation we propose is that by depressing homeostatic Reflexes at the NTS, noxious stimulation-evoked cardiorespiratory changes can be expressed and maintained, which may be essential for the survival of the animal.