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Julian F. R. Paton - One of the best experts on this subject based on the ideXlab platform.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.
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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
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Differential effects of angiotensin II on cardiorespiratory Reflexes mediated by nucleus tractus solitarii – a microinjection study in the rat
The Journal of Physiology, 1999Co-Authors: Julian F. R. Paton, Sergey KasparovAbstract:1The effect of microinjecting angiotensin II (ANGII) into the nucleus of the solitary tract (NTS) on both baroreceptor and peripheral chemoreceptor Reflexes was compared. 2Experiments were performed in a working heart-brainstem preparation of rat. Baroreceptors were stimulated by raising perfusion pressure and chemoreceptors were activated with aortic injections of sodium cyanide (0·025%, 25–75 μl). Reflex changes in phrenic nerve activity and heart rate were measured after bilateral NTS microinjection (50 nl) of ANGII (0·5–5000 fmol). 3NTS microinjection of 5 fmol ANGII elicited a transient (28·2 ± 6 s; mean ± s.e.m.) Bradycardia (-18 ± 3 beats min−1), and decreased phrenic nerve activity cycle length and amplitude (P < 0·05). At higher doses of ANGII a similar respiratory response was seen but heart rate changes were inconsistent. 4The baroreceptor Reflex Bradycardia was depressed significantly by NTS microinjections of ANGII (5–5000 fmol) in a dose-dependent manner with the Reflex gain decreasing from 1·7 ± 0·16 to 0·66 ± 0·1 beats min−1 mmHg−1 (P < 0·01) at 5000 fmol. Although the chemoreceptor Reflex Bradycardia was depressed at a low dose of ANGII (5 fmol), all higher doses (50–5000 fmol) produced a dose-dependent potentiation of the Reflex Bradycardia (maximally +64 ± 8%). The respiratory component was unaffected. The effects of ANGII on both Reflexes were blocked by an ANGII type 1 (AT1) receptor antagonist, losartan (20 μM). 5The potentiating action of ANGII on the chemoreceptor Reflex cardiac response was abolished by a neurokinin type 1 (NK1) receptor blocker (CP-99,994, 5 μM) but this had no effect on the baroreceptor Reflex. 6AT1 receptors in the NTS can depress the baroreceptor Reflex Bradycardia which is independent of NK1 receptors. The ANGII effect on the cardiac component of the chemoreceptor Reflex is bi-directional being inhibited at low concentrations and potentiated at higher concentrations; the latter involves NK1 receptors and presumably results from release of substance P.
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K+ channel blockade in the NTS alters efficacy of two cardiorespiratory Reflexes in vivo
The American journal of physiology, 1998Co-Authors: James W Butcher, Julian F. R. PatonAbstract:We investigated the role of potassium conductances in the nucleus of the solitary tract (NTS) in determining the efficacy of the baroreceptor and cardiopulmonary Reflexes in anesthetized rats. The baroreceptor Reflex was elicited with an intravenous injection of phenylephrine to evoke a Reflex Bradycardia, and the cardiopulmonary Reflex was evoked with a right atrial injection of phenylbiguanide. Microinjection of two Ca-dependent potassium channel antagonists (apamin and charybdotoxin) into the NTS potentiated the baroreceptor Reflex Bradycardia. This may reflect the increased neuronal excitability observed previously in vitro with these blockers. In contrast, the Ca-dependent potassium channel antagonists attenuated the cardiopulmonary Reflex, whereas voltage-dependent potassium channel antagonists (4-aminopyridine and dendrotoxin) attenuated both the baro- and cardiopulmonary Reflexes when microinjected into the NTS. The possibility that the Reflex attenuation observed indicates a predominant distribution of certain potassium channels on γ-aminobutyric acid interneurons is discussed.
Pedro Boscan - One of the best experts on this subject based on the ideXlab platform.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.
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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
Duk Kyung Kim - One of the best experts on this subject based on the ideXlab platform.
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Analysis of factors related to vagally mediated Reflex Bradycardia during gastrectomy.
Journal of anesthesia, 2015Co-Authors: Duk Kyung Kim, Hyun Joo Ahn, Seung Won Lee, Ji Won ChoiAbstract:Purpose Because vagally mediated Reflex Bradycardia occurs frequently during gastrectomy and is potentially harmful, we compared the incidence of clinically significant Reflex Bradycardia between patients undergoing laparoscopic gastrectomy (LG) and open gastrectomy (OG) and examined whether the type of surgery (OG vs. LG) was an independent risk factor for clinically significant Reflex Bradycardia.
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Dose fentanyl injection for blunting the hemodynamic response to intubation increase the risk of Reflex Bradycardia during major abdominal surgery
Korean journal of anesthesiology, 2012Co-Authors: Jin-kyoung Kim, Jung-min Park, Cheol-hee Lee, Duk Kyung KimAbstract:Background: Although supplemental fentanyl has been widely used to blunt the hemodynamic responses to laryngoscopic intubation, its residual vagotonic effect may increase the risk of Reflex Bradycardia. We compared the incidence and severity of significant Reflex Bradycardia after a bolus injection of equivalent doses of fentanyl and remifentanil (control drug). Methods: In this prospective, randomized, doubleblind study, 220 adult patients undergoing major abdominal surgery were randomly assigned to receive fentanyl (1.5 μg/kg) or remifentanil (1.5 μg/kg). No anticholinergic prophylaxis was administered. Symptomatic Reflex Bradycardia was defined as a sudden decrease in heart rate to < 50 beats per minute (bpm) or to 50-59 bpm associated with a systolic arterial pressure < 70 mmHg in connection with surgical maneuvers. If Bradycardia or hypotension developed, atropine or ephedrine was administered following a predefined treatment protocol. Results: In total, 188 subjects (remifentanil, 95; fentanyl, 93) were included. The proportion of subjects with symptomatic Reflex Bradycardia in the fentanyl group was similar to that in the remifentanil group (30.1% vs. 28.4%, respectively). Atropine and/or ephedrine were needed similarly in both groups. The differences between the group of 55 patients who presented with symptomatic Reflex Bradycardia were not statistically significant with respect to the lowest heart rate, anesthetic depthrelated data (bispectral index and endtidal sevoflurane concentration), or the proportion of causative surgical maneuvers. Conclusions: Fentanyl (1.5 μg/kg) administered intravenously during anesthetic induction is unlikely to increase the incidence and severity of significant Reflex Bradycardia in patients undergoing major abdominal surgery. (Korean J Anesthesiol 2012; 63: 402408)
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comparison of desflurane and sevoflurane anaesthesia in relation to the risk of vagally mediated Reflex Bradycardia during gastrectomy
Journal of International Medical Research, 2012Co-Authors: Young Joo, Byung Seop Shin, Eunah Cho, Duk Kyung KimAbstract:OBJECTIVE This study compared the risk of clinically significant Reflex Bradycardia during anaesthesia with sevoflurane or desflurane in patients undergoing gastrectomy. METHODS In this randomized prospective study, 100 patients undergoing gastrectomy were assigned to receive sevoflurane (n=50) or desflurane (n=50) anaesthesia. No anticholinergic prophylaxis was administered. Symptomatic Reflex Bradycardia was defined as a sudden decrease in heart rate to <50 beats/min, or a decrease to 50-59 beats/min if associated with a systolic arterial pressure of 70 mmHg in response to surgical manoeuvres. If Reflex Bradycardia developed, atropine or ephedrine were administered according to a predefined treatment protocol. RESULTS Data from 85 patients were available for analysis. The proportion of patients with symptomatic Reflex Bradycardia in the sevoflurane and desflurane groups was similar (69.0% versus 55.8%, respectively) and both groups required a similar amount of atropine and/or ephedrine. CONCLUSIONS Clinically significant Reflex Bradycardia occurred with a relatively high frequency during gastrectomy. Although desflurane is associated with sympathetic activation, it did not provide a protective effect against vagally mediated Reflex Bradycardia during gastrectomy compared with sevoflurane.
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Comparison of Desflurane and Sevoflurane Anaesthesia in Relation to the Risk of Vagally Mediated Reflex Bradycardia during Gastrectomy
The Journal of international medical research, 2012Co-Authors: Young Joo, Byung Seop Shin, Eunah Cho, Duk Kyung KimAbstract:OBJECTIVE This study compared the risk of clinically significant Reflex Bradycardia during anaesthesia with sevoflurane or desflurane in patients undergoing gastrectomy. METHODS In this randomized prospective study, 100 patients undergoing gastrectomy were assigned to receive sevoflurane (n=50) or desflurane (n=50) anaesthesia. No anticholinergic prophylaxis was administered. Symptomatic Reflex Bradycardia was defined as a sudden decrease in heart rate to
Ruben D. Buñag - One of the best experts on this subject based on the ideXlab platform.
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Baroreceptor Reflex Impairment and Mild Hypertension in Rats with
2016Co-Authors: Dietary-induced Obesity, Ruben D. Buñag, Lea Eriksson, D KrizsanAbstract:Cardiovascular dysfunction associated with obesity was assessed by comparing rats that had been maintained on a regular or high fat diet since weaning. Rats on the high fat diet not only gained weight faster than age-matched controls but also had higher systolic and mean pressures. Development of mild hypertension in obese rats was first detected by indirect tail-cuff measurement and confirmed later by recording intra-arterial pressures directly from indwelling femoral catheters. To assess baroreceptor Reflex sensitivity, Reflex heart rate responses were elicited by lowering blood pressure with sodium nitroprusside or elevating it with phenylephrine. Initial tests showed that, although Reflex tachycardia during depressor responses to sodium nitroprusside did not differ between groups, Reflex Bradycardia during pressor responses to phenylephrine was weaker in obese than in control rats. Underlying autonomic mechanisms were then examined by repetition of baroreceptor Reflex tests after cholinergic blockade with methylatropine or /3-adrenergic blockade with propranolol. Reflex tachycardia was equally inhibited in both groups by either antagonist. By contrast, Reflex Bradycardia was reduced more in obese than in control rats by /3-adrenergic blockade but was equally reduced by cholinergic blockade. Because residual responses after /3-adrenergi
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Short-term lisinopril treatment in old rats worsens impairment of angiotensin-induced Reflex Bradycardia.
Journal of cardiovascular pharmacology, 1997Co-Authors: Elizabeth Montemayor, Jennifer R. Mellick, Laszlo Kerecsen, Ruben D. BuñagAbstract:To determine how short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor affects drug-induced Reflex Bradycardia at different ages in conscious rats, we compared the magnitude of drug-induced Reflex Bradycardia before and after injecting bolus intravenous doses of lisinopril, 1 mg/100 g, in male Sprague-Dawley rats aged 4 (young) or 19 (old) months. Anesthetic artifacts were avoided by recording all drug-induced cardiovascular responses from femoral arterial cannulas implanted 1 week earlier. For eliciting Reflex Bradycardia, blood pressure was increased by graded intravenous infusion of angiotensin or phenylephrine. Impairment of Reflex Bradycardia in old rats occurred only during pressor responses to angiotensin but not when blood pressure was equally increased with phenylephrine. Subsequent administration of lisinopril affected neither pressor and Reflex bradycardic responses to phenylephrine nor pressor responses to angiotensin. However, contrary to the baroReflex enhancement described previously by others, the Reflex Bradycardia induced by angiotensin was reduced by lisinopril treatment but only in old and not in young rats. Thus our results indicate that whereas angiotensin-induced Reflex Bradycardia was already impaired in old rats before lisinopril was given, it was reduced further after short-term lisinopril treatment.
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Age-related reduction of Reflex Bradycardia in conscious rats by catecholaminergic nucleus tractus solitarius lesions.
Mechanisms of ageing and development, 1993Co-Authors: Hiroshi Itoh, Ruben D. BuñagAbstract:To determine whether catecholaminergic lesions in the nucleus tractus solitarius (NTS) have age-related baroReflex effects, we compared conscious 3-month- and 14-month-old rats pretreated with either 6-hydroxydopamine (6-OHDA) or vehicle injected into the NTS. Body weights fell immediately in both age groups, but after 2 weeks the weight loss persisted only in 14-month-old rats. Mean pressures and heart rates, though diminished after 3 days, were later elevated slightly in 3-month- but not in 14-month-old rats. Two weeks after 6-OHDA pretreatment, Reflex tachycardia was reduced in both age groups, but Reflex Bradycardia was reduced only in 3-month-old and not in 14-month-old rats. Corresponding changes in vehicle-treated rats were not significant. Because 6-OHDA induced lesions in the NTS inhibited Reflex Bradycardia selectively at 3 but not at 14 months of age, our results suggest that catecholaminergic mechanisms in the NTS for regulating Reflex Bradycardia become impaired with age.
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Autonomic regulation of Reflex Bradycardia in rats declines with age.
Experimental gerontology, 1991Co-Authors: Donna L. Barringer, Ruben D. BuñagAbstract:Abstract Heart rate responses, elicited Reflexly by elevating blood pressure with phenylephrine or lowering it with sodium nitroprusside, were compared in groups of rats aged 4 and 14 months. All tests were done while the rats were awake to avoid artefacts due to anesthesia. Parasymphatetic and sympathetic contributions were assessed by repeating baroReflex tests after cholinergic blockade with atropine or β-adrenergic blockade with propranolol. Magnitude of Reflex Bradycardia was initially smaller in the 14-month-old rats than in the younger rats thereby indicating that baroReflex sensitivity had diminished with age. After β-adrenergic or cholinergic blockade, adjusted means (obtained by covariance analysis) for Reflex tachycardia did not differ significantly between rat groups, but those for Reflex Bradycardia were significantly smaller in the 14-month-old rats than in the younger rats. Selective attenuation of Reflex Bradycardia after either cholinergic or β-adrenergic blockade indicates that concurrent parasympathetic activation and sympathetic withdrawal during Reflex Bradycardia were also reduced in 14-month-old rats. These results suggest that as autonomic mediation of Reflex Bradycardia diminishes with age, old rats may no longer be able to slow the heart as easily whenever blood pressure rises, but they can still accelerate it whenever blood pressure falls.
Benedito H Machado - One of the best experts on this subject based on the ideXlab platform.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.
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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, 2002Co-Authors: Julian F. R. Paton, Patricia M. De Paula, K. Michael Spyer, Benedito H Machado, Pedro BoscanAbstract: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.