Activity patterns of cardiac vagal motoneurons in rat  nucleus ambiguus

Rentero, N.; Cividjian, Andrei; Trevaks, David; Pequignot, J. M.; Quintin, Luc; McAllen, Robin M.

doi:10.1152/ajpregu.00271.2002

Cited by 47 publications

(58 citation statements)

References 41 publications

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“…The ventilatory modulation of tail SNA could have been due to a direct reflex action of pulmonary afferents, or secondary to entrainment by the ventilator of central respiratory drive (31), or of an intrinsically rhythmic firing pattern of tail vasoconstrictor neurons (9). Respiratory modulation of iBAT activity has been described by Morrison (17), although under his experimental conditions, this was only evident in vagotomized rats.…”

Section: Discussionmentioning

confidence: 89%

“…In our experiments, however, rats with intact vagi showed ventilatory modulation of BAT SNA, presumably because of subtle differences in the experimental preparation. We cannot distinguish whether this was because of direct reflex modulation by lung inflation receptors or because of central respiratory drive, which is normally entrained to the ventilatory cycle in rats with intact vagi (31). The significance of finding respiratory-related modulation of both of these cold-defense neural pathways remains unclear.…”

Section: Discussionmentioning

confidence: 93%

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Comparison between two rat sympathetic pathways activated in cold defense

Ootsuka

McAllen²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 93%

Comparison between two rat sympathetic pathways activated in cold defense

Ootsuka

McAllen²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The craniovagal cardiac branch was identified by its location and its ability to cause bradycardia when stimulated (20 -50 Hz, 2-7 V, 0.05 ms) (40). A pair of electrodes made from Teflon-coated 1,250 m silver wire, bared at the tips, was placed under the branch.…”

Section: Ratsmentioning

confidence: 99%

“…Using data previously collected from healthy human volunteers (37), sBRS (13) and xBRS (56) algorithms were used to test this prediction. To generalize the findings in a second species and to pursue the mechanisms responsible, data on HR and the activity of cardiac vagal motoneurons (CVM) (32,40,53) were taken from a published study on anesthetized rats (53), reanalyzed, and supplemented with further experiments. These steps allowed the central and efferent components of the reflex pathway to be studied independently of each other, clarifying the site and mode of action of clonidine on cardiac baroreflex delay.…”

mentioning

confidence: 99%

Effect of clonidine on cardiac baroreflex delay in humans and rats

Cividjian

Toader

Wesseling

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Cividjian A, Toader E, Wesseling KH, Karemaker JM, McAllen R, Quintin L. Effect of clonidine on cardiac baroreflex delay in humans and rats. Am J Physiol Regul Integr Comp Physiol 300: R949-R957, 2011. First published January 26, 2011 doi:10.1152/ajpregu.00438.2010The delay between rising systolic blood pressure (SBP) and baroreflex bradycardia has been found to increase when vagal tone is low. The ␣2-agonist clonidine increases cardiac vagal tone, and this study tested how it affects . In eight conscious supine human volunteers clonidine (6 g/kg po) reduced , assessed both by cross correlation baroreflex sensitivity and sequence methods (both P Ͻ 0.05). Experiments on urethane-anaesthetized rats reproduced the phenomenon and investigated the underlying mechanism. Heart rate (HR) responses to increasing SBP produced with an arterial balloon catheter showed reduced (P Ͻ 0.05) after clonidine (100 g/kg iv). The central latency of the reflex was unaltered, however, as shown by the unchanged timing with which antidromically identified cardiac vagal motoneurons (CVM) responded to the arterial pulse. Testing the latency of the HR response to brief electrical stimuli to the right vagus showed that this was also unchanged by clonidine. Nevertheless, vagal stimuli delivered at a fixed time in the cardiac cycle (triggered from the ECG R-wave) slowed HR with a 1-beat delay in the baseline state but a 0-beat delay after clonidine (n ϭ 5, P Ͻ 0.05). This was because clonidine lengthened the diastolic period, allowing the vagal volleys to arrive at the heart just in time to postpone the next beat. Calculations indicate that naturally generated CVM volleys in both humans and rats arrive around this critical time. Clonidine thus reduces not by changing central or efferent latencies but simply by slowing the heart. sequences; lag; latency; cardiac vagal motoneurons; ␣ 2-agonist THE GAIN OF THE ARTERIAL baroreceptor-heart rate reflex (cardiac baroreflex) has been calculated from the relationship between spontaneous (10, 13) or drug-induced (47) increases in systolic blood pressure (SBP) and the accompanying decrease in heart rate (HR). In humans, the best correlations were initially obtained by relating cardiac intervals to the preceding SBP (delay ϭ 1 beat) (47), although later studies (14, 38) found a delay of 0 beat was appropriate in subjects with lower initial HRs. In unanesthetized rats, delays of between 2 and 14 beats gave the best correlation for spontaneous baroreflex measurements (35); the best fit for tachycardic responses was 2 to 3 beats longer than that for bradycardic responses (35). The sequence technique of baroreflex sensitivity (sBRS) (13) traditionally uses a constant delay ϭ 1 beat to measure spontaneous baroreflex slope in humans, although the method may be applied using delays of any whole number of beats. This approach has been expanded to give a near-continuous assessment of the slope of the cardiac baroreflex [time-domain cross-correlation BRS (xBRS)] (56). The algorithm of xBRS (56) adjusts in seconds...

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“…Within the NA, the rhythmic activity of CVPN is dependent on excitatory and inhibitory synaptic inputs (22,44), including ongoing baroreflex [mediated via the nucleus of the solitary tract (NTS)] and respiratory input (9,33). Phasic inhibition of inhibitory input to CVPN is critical for producing reflexmediated bradycardia (46).…”

mentioning

confidence: 99%

Impaired serotonergic regulation of heart rate may underlie reduced baroreflex sensitivity in an animal model of depression

Hildreth¹,

Padley²,

Pilowsky³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Hildreth CM, Padley JR, Pilowsky PM, Goodchild AK. Impaired serotonergic regulation of heart rate may underlie reduced baroreflex sensitivity in an animal model of depression. Am J Physiol Heart Circ Physiol 294: H474-H480, 2008. First published November 9, 2007 doi:10.1152/ajpheart.01009.2007.-Serotonin (5-HT) is crucial to normal reflex vagal modulation of heart rate (HR). Reduced baroreflex sensitivity [spontaneous baroreflex sensitivity (sBRS)] and HR variability (HRV) reflect impaired neural, particularly vagal, control of HR and are independently associated with depression. In conscious, telemetered Flinders-Sensitive Line (FSL) rats, a wellvalidated animal model of depression, we tested the hypothesis that cardiovascular regulatory abnormalities are present and associated with deficient serotonergic control of reflex cardiovagal function. In FSL rats and control Flinders-Resistant (FRL) and Sprague-Dawley (SD) rat strains, diurnal measurements of HR, arterial pressure (AP), activity, sBRS, and HRV were made. All strains had normal and similar diurnal variations in HR, AP, and activity. In FRL rats, HR was elevated, contributing to the reduced HRV and sBRS in this strain. In FSL rats, sBRS and high-frequency power HRV were reduced during the night, indicating reduced reflex cardiovagal activity. The ratio of low-to high-frequency bands of HRV was increased in FSL rats, suggesting a relative predominance of cardiac sympathetic and/or reflex activity compared with FRL and SD rats. These data show that conscious FSL rats have cardiovascular regulatory abnormalities similar to depressed humans. Acute changes in HR, AP, temperature, and sBRS in response to 8-hydroxy-2-(di-npropylamino)tetralin, a 5-HT 1A, 5-HT1B, and 5-HT7 receptor agonist, were also determined. In FSL rats, despite inducing an exaggerated hypothermic effect, 8-hydroxy-2-(di-n-propylamino)tetralin did not decrease HR and AP or improve sBRS, suggesting impaired serotonergic neural control of cardiovagal activity. These data suggest that impaired serotonergic control of cardiac reflex function could be one mechanism linking reduced sBRS to increased cardiac risk in depression.serotonin-1A receptors; 8-hydroxy-2-(di-n-propylamino)tetralin; Flinders Sensitive Line rat; vagus; telemetry TONIC AND REFLEX CONTROL of heart rate (HR) is dependent on the balance of parasympathetic (vagal) and sympathetic neural input. Disruption of this balance, through a decrease in vagal tone or an increase in sympathetic tone, leads to cardiac dysfunction and/or arrhythmias (35,43).Tonic levels of cardiovagal activity and, consequently, the level of resting HR are controlled by the activity of cardiac vagal preganglionic neurons (CVPN) located in the nucleus ambiguus (NA) and dorsal motonucleus of the vagus (44). Within the NA, the rhythmic activity of CVPN is dependent on excitatory and inhibitory synaptic inputs (22, 44), including ongoing baroreflex [mediated via the nucleus of the solitary tract (NTS)] and respiratory input (9, 33). Phasic inhibition of inhibitory...

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Activity patterns of cardiac vagal motoneurons in rat nucleus ambiguus

Cited by 47 publications

References 41 publications

Comparison between two rat sympathetic pathways activated in cold defense

Comparison between two rat sympathetic pathways activated in cold defense

Effect of clonidine on cardiac baroreflex delay in humans and rats

Impaired serotonergic regulation of heart rate may underlie reduced baroreflex sensitivity in an animal model of depression

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