The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
David Robertson - One of the best experts on this subject based on the ideXlab platform.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:BACKGROUND: The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of Baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the Baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although Baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of Baroreflex failure requires specific strategies, which may lead to successful control.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:Background— The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. Methods and Results— Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-t...
Caroline Sevozcouche - One of the best experts on this subject based on the ideXlab platform.
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rostral cuneiform nucleus and the defence reaction direct and indirect midbrain medullary 5 ht mechanisms in Baroreflex inhibition
British Journal of Pharmacology, 2021Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:Background and purpose Activation of the defence reaction inhibits the Baroreflex response via the intermediate rostro-ventromedial medulla (B3 raphe) and nucleus tractus solitarius (NTS). Our aim was to determine whether and how Baroreflex inhibition, induced by the disinhibition of the rostral cuneiform nucleus (part of the defence pathway), involves 5-HT neurons in B3 and 5-HT3 receptors in the NTS. Experimental approach We performed immunohistochemistry and anatomical experiments to determine whether raphe 5-HT cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe 5-HT neurotransmission and NTS 5-HT3 receptors on cuneiform-induced inhibition of the Baroreflex cardiac response were also analysed. Key results Bicuculline, microinjected into the rostral cuneiform nucleus, induced an increase of double-labelled Fos-5-HT-IR cells in both the lateral paragigantocellular nucleus (LPGi) and raphe magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin injected into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not raphe magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a selective 5-HT1A receptor agonist. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after NTS microinjection of the 5-HT3 receptor antagonist granisetron and in 5-HT3 receptor knockout mice. Conclusion and implications The rostral cuneiform nucleus participates in the defence inhibition of the Baroreflex bradycardia via direct activation of the LPGi and via a projection to the raphe magnus to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
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rostral cuneiform nucleus and the defense reaction direct and indirect midbrain medullary serotonin mechanisms in Baroreflex inhibition
British Journal of Pharmacology, 2021Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:BACKGROUND AND PURPOSE Activation of the defence reaction inhibits the Baroreflex response via the intermediate rostro-ventromedial medulla (B3 raphe) and nucleus tractus solitarius (NTS). Our aim was to determine whether and how Baroreflex inhibition, induced by the disinhibition of the rostral cuneiform nucleus (part of the defence pathway), involves 5-HT neurons in B3 and 5-HT3 receptors in the NTS. EXPERIMENTAL APPROACH We performed immunohistochemistry and anatomical experiments to determine whether raphe 5-HT cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe 5-HT neurotransmission and NTS 5-HT3 receptors on cuneiform-induced inhibition of the Baroreflex cardiac response were also analysed. KEY RESULTS Bicuculline, microinjected into the rostral cuneiform nucleus, induced an increase of double-labelled Fos-5-HT-IR cells in both the lateral paragigantocellular nucleus (LPGi) and raphe magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin injected into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not raphe magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a selective 5-HT1A receptor agonist. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after NTS microinjection of the 5-HT3 receptor antagonist granisetron and in 5-HT3 receptor knockout mice. CONCLUSION AND IMPLICATIONS The rostral cuneiform nucleus participates in the defence inhibition of the Baroreflex bradycardia via direct activation of the LPGi and via a projection to the raphe magnus to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
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rostral cuneiform nucleus and the defense reaction direct and indirect midbrain medullary serotonin mechanisms in Baroreflex inhibition
Authorea Preprints, 2020Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:Background and Purpose: The activation of the defense reaction inhibits the Baroreflex response through the B3 and nucleus tractus solitarius (NTS) regions. Our aim was to determine whether and how Baroreflex inhibition induced by the disinhibition of the rostral cuneiform nucleus, part of the defense pathway, involves serotonin cells in B3 and 5-HT3 receptors in the NTS. Experimental Approach: We performed immunohistochemistry and anatomical experiments to determine whether raphe serotonin cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe serotonin transmission and NTS 5-HT3 receptors, on cuneiform-induced inhibition of the Baroreflex cardiac response, were also analyzed. Key Results: Bicuculline microinjected into the rostral cuneiform nucleus induced an increase of double labeled Fos-5-HT IR cells in both the LPGi and Raphe Magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not Raphe Magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a specific agonist for 5-HT1A receptors. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after microinjection of a 5-HT3 receptor antagonist (granisetron) into the NTS or in 5-HT3 receptor knock-out mice. Conclusion and Implications: In conclusion, the rostral cuneiform nucleus participates in the defense inhibition of the Baroreflex bradycardia via direct activation of the LPGi and a relay to the Raphe Magnus, to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
Terry Ketch - One of the best experts on this subject based on the ideXlab platform.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:BACKGROUND: The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of Baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the Baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although Baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of Baroreflex failure requires specific strategies, which may lead to successful control.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:Background— The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. Methods and Results— Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-t...
Florence Netzer - One of the best experts on this subject based on the ideXlab platform.
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rostral cuneiform nucleus and the defence reaction direct and indirect midbrain medullary 5 ht mechanisms in Baroreflex inhibition
British Journal of Pharmacology, 2021Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:Background and purpose Activation of the defence reaction inhibits the Baroreflex response via the intermediate rostro-ventromedial medulla (B3 raphe) and nucleus tractus solitarius (NTS). Our aim was to determine whether and how Baroreflex inhibition, induced by the disinhibition of the rostral cuneiform nucleus (part of the defence pathway), involves 5-HT neurons in B3 and 5-HT3 receptors in the NTS. Experimental approach We performed immunohistochemistry and anatomical experiments to determine whether raphe 5-HT cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe 5-HT neurotransmission and NTS 5-HT3 receptors on cuneiform-induced inhibition of the Baroreflex cardiac response were also analysed. Key results Bicuculline, microinjected into the rostral cuneiform nucleus, induced an increase of double-labelled Fos-5-HT-IR cells in both the lateral paragigantocellular nucleus (LPGi) and raphe magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin injected into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not raphe magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a selective 5-HT1A receptor agonist. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after NTS microinjection of the 5-HT3 receptor antagonist granisetron and in 5-HT3 receptor knockout mice. Conclusion and implications The rostral cuneiform nucleus participates in the defence inhibition of the Baroreflex bradycardia via direct activation of the LPGi and via a projection to the raphe magnus to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
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rostral cuneiform nucleus and the defense reaction direct and indirect midbrain medullary serotonin mechanisms in Baroreflex inhibition
British Journal of Pharmacology, 2021Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:BACKGROUND AND PURPOSE Activation of the defence reaction inhibits the Baroreflex response via the intermediate rostro-ventromedial medulla (B3 raphe) and nucleus tractus solitarius (NTS). Our aim was to determine whether and how Baroreflex inhibition, induced by the disinhibition of the rostral cuneiform nucleus (part of the defence pathway), involves 5-HT neurons in B3 and 5-HT3 receptors in the NTS. EXPERIMENTAL APPROACH We performed immunohistochemistry and anatomical experiments to determine whether raphe 5-HT cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe 5-HT neurotransmission and NTS 5-HT3 receptors on cuneiform-induced inhibition of the Baroreflex cardiac response were also analysed. KEY RESULTS Bicuculline, microinjected into the rostral cuneiform nucleus, induced an increase of double-labelled Fos-5-HT-IR cells in both the lateral paragigantocellular nucleus (LPGi) and raphe magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin injected into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not raphe magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a selective 5-HT1A receptor agonist. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after NTS microinjection of the 5-HT3 receptor antagonist granisetron and in 5-HT3 receptor knockout mice. CONCLUSION AND IMPLICATIONS The rostral cuneiform nucleus participates in the defence inhibition of the Baroreflex bradycardia via direct activation of the LPGi and via a projection to the raphe magnus to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
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rostral cuneiform nucleus and the defense reaction direct and indirect midbrain medullary serotonin mechanisms in Baroreflex inhibition
Authorea Preprints, 2020Co-Authors: Florence Netzer, Caroline SevozcoucheAbstract:Background and Purpose: The activation of the defense reaction inhibits the Baroreflex response through the B3 and nucleus tractus solitarius (NTS) regions. Our aim was to determine whether and how Baroreflex inhibition induced by the disinhibition of the rostral cuneiform nucleus, part of the defense pathway, involves serotonin cells in B3 and 5-HT3 receptors in the NTS. Experimental Approach: We performed immunohistochemistry and anatomical experiments to determine whether raphe serotonin cells expressing Fos were directly targeted by the rostral cuneiform nucleus. The effect of blocking raphe serotonin transmission and NTS 5-HT3 receptors, on cuneiform-induced inhibition of the Baroreflex cardiac response, were also analyzed. Key Results: Bicuculline microinjected into the rostral cuneiform nucleus induced an increase of double labeled Fos-5-HT IR cells in both the LPGi and Raphe Magnus. The anterograde tracer Phaseolus vulgaris leucoaggutinin into the rostral cuneiform nucleus revealed a dense projection to the LPGi but not Raphe Magnus. Cuneiform-induced Baroreflex inhibition was prevented by B3 injection of 8-OH-DPAT, a specific agonist for 5-HT1A receptors. Cuneiform disinhibition also failed to inhibit the Baroreflex bradycardia after microinjection of a 5-HT3 receptor antagonist (granisetron) into the NTS or in 5-HT3 receptor knock-out mice. Conclusion and Implications: In conclusion, the rostral cuneiform nucleus participates in the defense inhibition of the Baroreflex bradycardia via direct activation of the LPGi and a relay to the Raphe Magnus, to activate NTS 5-HT3 receptors and inhibit second-order Baroreflex neurons. These data bring new insights in primary and secondary mechanisms involved in vital Baroreflex prevention during stress.
R M Robertson - One of the best experts on this subject based on the ideXlab platform.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:BACKGROUND: The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. METHODS AND RESULTS: Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of Baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the Baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest. CONCLUSIONS: Although Baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of Baroreflex failure requires specific strategies, which may lead to successful control.
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four faces of Baroreflex failure hypertensive crisis volatile hypertension orthostatic tachycardia and malignant vagotonia
Circulation, 2002Co-Authors: Terry Ketch, Italo Biaggioni, R M Robertson, David RobertsonAbstract:Background— The Baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In Baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences. Methods and Results— Impairment of the Baroreflex may produce an unusually broad spectrum of clinical presentations; with acute Baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-t...
