Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

McCloskey, D.I.; Potter, Erica K.

doi:10.1113/jphysiol.1981.sp013780

Cited by 19 publications

(15 citation statements)

References 26 publications

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“…Neural activity in the filaments containing one or a few active fibres were recorded with preamplifiers (Neurolog NL103/106: band pass between 10 Hz and 1 kHz), a loudspeaker and storage oscilloscope. Criteria for definition of single-unit activity were those used by McCloskey & Potter (1981). Records of cardiac vagal efferent activity were obtained by direct photography from the oscilloscope screen.…”

Section: Methodsmentioning

confidence: 99%

“…Each animal was prepared for recordings from cardiac vagal efferent fibres as described in the preceding paper (McCloskey & Potter, 1981). Briefly, the entire pharynx and larynx were removed and the right cervical vagus was divided into filaments.…”

Section: Methodsmentioning

confidence: 99%

“…70C). DISCUSSION It is known that in the inspiratory phase of breathing tonic activity in cardiac vagal efferent nerves is inhibited (Anrep et al 1936a, b;Rijlant, 1936;Jewett, 1964;Davidson et al 1976;McCloskey & Potter, 1981). Stimuli which can evoke cardiac vagal activity usually fail to do so when delivered in the inspiratory phase of breathing (Koepchen et al 1961;Haymet & McCloskey, 1975;Neil & Palmer, 1975;Lopes & Palmer, 1976;Gandevia et al 1978a, b).…”

Section: Inhibition Of Cardiodepressor Reflexesmentioning

confidence: 99%

“…These prolongations of response are mainly due to the properties of the central relays between baroreceptor inputs and vagal motoneurones, and cannot be ascribed solely to temporal dispersion of afferent volleys along the carotid sinus nerve (McCloskey & Potter, 1981). Intracarotid pressure pulses were chosen as it is known that these selectively activate arterial baroreceptors for the duration of the rise in pressure (Haymet & McCloskey, 1975).…”

Section: Inhibition Of Cardiodepressor Reflexesmentioning

confidence: 99%

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Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Potter¹

1981

The Journal of Physiology

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SUMMARY1. Single and few-fibre cardiac efferent filaments were dissected from the cervical vagus nerve of dogs anaesthetized with chloralose and paralysed with pancuronium.2. Brief selective baroreceptor or chemoreceptor stimuli, given during the expiratory phase ofthe central respiratory cycle and while the lungs were motionless, evoked trains of action potentials in cardiac vagal efferent fibres. These vagal responses outlasted the duration of the stimuli by 1-3 s.3. Briefselective baroreceptororchemoreceptorstimuli given during the inspiratory phase of the central respiratory cycle (monitored as phrenic discharge) but while the lungs were motionless, failed to evoke reflex increases in discharge. Background vagal discharge was also inhibited during central inspiratory activity.4. Brief baroreceptor or chemoreceptor stimuli given during lung inflation but in the expiratory phase of the central respiratory cycle (phrenic silence), also failed to evoke any reflex increase in discharge, but left resting vagal tone relatively unaffected. Only when vagal tone was high was it markedly inhibited by lung inflation, in the absence of central inspiratory activity.5. A point of contrast between the inhibitory effects of lung inflation and of central inspiratory activity is that both tonic and reflexly evoked vagal discharge are inhibited during central inspiratory activity, but lung inflation more markedly inhibits reflexly evoked vagal discharge than tonic vagal discharge. 6. A model is suggested to explain the different mechanisms of inhibition by lung inflation and by central inspiratory activity.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Inhibition Of Cardiodepressor Reflexesmentioning

confidence: 99%

Section: Inhibition Of Cardiodepressor Reflexesmentioning

confidence: 99%

See 2 more Smart Citations

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Potter¹

1981

The Journal of Physiology

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“…However, it is difficult to equate a given nerve stimulation frequency with a carotid sinus pressure stimulus that physiologically activates baroreceptors. Furthermore, electrical stimulation of carotid sinus baroreceptor afferent fibers produces both excitatory and inhibitory reflex effects on cardiac vagal efferent fibers (McCloskey and Potter, 1981), in contrast to only excitatory effects reported with functional pressure stimulation of baroreceptors (Potter, 1981). It is also possible that much of the conflicting coronary flow data can be explained by alterations in myocardial metabolism, secondary to changes in heart rate and aortic pressure, in response to activation of the baroreceptor reflex.…”

mentioning

confidence: 99%

Carotid baroreceptor reflex coronary vasodilation in the dog.

Ito

Feigl²

1985

Circulation Research

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SUMMARY. The hypothesis that neurally mediated coronary vasodilation occurs as part of the carotid baroreceptor reflex was investigated. The left main coronary artery was cannulated and perfused at constant pressure (100 mm Hg) in closed-chest, chloralose-anesthetized dogs. The heart was paced at a constant rate between 60 and 70 beats/min after atrioventricular heart block. Propranolol (1 mg/kg) was given to prevent j3-receptor-mediated alterations in contractility. Aortic blood pressure was stabilized with a blood reservoir. The aortic depressor nerves were cut bilaterally to prevent the buffering influence of aortic arch baroreceptors on the carotid baroreceptor reflex. The carotid sinuses were vascularly isolated and perfused with arterial blood at controlled pressures. Under these conditions, a step change in carotid sinus pressure from 70 to 210 mm Hg produced a 0.29 ml/min per g increase in coronary flow above control and a 10 mm Hg increase in coronary sinus blood oxygen tension. A step in carotid sinus pressure from 70 to 150 mm Hg resulted in a flow increase of 0.13 ml/min per g and a coronary sinus oxygen tension increase of 5.3 mm Hg relative to prestimulation values. Atropine (0.5 mg/kg, iv) blocked most of the reflex coronary vasodilation, indicating a parasympathetic component, and the addition of adrenergic a-receptor blockade with phenoxybenzamine (0.25 mg/kg, ic) abolished the remaining response, demonstrating sympathetic participation. The reflex nature of the coronary response was confirmed with carotid sinus denervation and vagotomy. It is concluded that carotid sinus hypertension results in a graded reflex neural coronary vasodilation independent of myocardial metabolic factors. The major component is due to activation of parasympathetic coronary vasodilator fibers, but there is also inhibition of sympathetic vasoconstrictor fibers. (Circ Res 56: 486-495, 1985) PREVIOUS studies have demonstrated that adrenergic a-receptor coronary vasoconstriction can be reflexly elicited by carotid sinus hypotension (Feigl, 1968(Feigl, , 1983DiSalvo et al., 1971;Limet et al., 1975;Powell and Feigl, 1979;Ely et al., 1981). However, the reflex response to carotid sinus hypertension is less clear. Both coronary vasoconstriction (DiSalvo et al., 1971) and coronary vasodilation (Limet et al., 1975) have been observed during acute elevations in carotid sinus pressure. Coronary vasodilation during the elevation of aortic pressure has also been attributed to the carotid baroreflex (White et al., 1976). Electrical stimulation of the afferent carotid sinus nerve has been employed to mimic carotid sinus hypertension, and either coronary vasoconstriction (Falicov et al., 1970) or vasodilation (Vatner et al., 1970;Hackett et al., 1972;Religa et al., 1972;Solti et al., 1975) has been observed. However, it is difficult to equate a given nerve stimulation frequency with a carotid sinus pressure stimulus that physiologically activates baroreceptors. Furthermore, electrical stimulation of carotid sinus baroreceptor affe...

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Synaptic morphology of substance P terminals on catecholamine neurons in the commissural subnucleus of the nucleus tractus solitarii in the rat

Chen

Cusick

Weber

et al. 1994

Microscopy Res & Technique

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The ultrastructure of substance P-containing nerve terminals synapsing on catecholamine neurons in the rat commissural subnucleus of the nucleus tractus solitarii (NTScom) was studied using a double immunocytochemical labeling technique. Although there were numerous tyrosine hydroxylase-immunoreactive (TH-I) somata present, substance P immunoreactive (SP-I) cell bodies were only occasionally found in the NTScom. At the light microscopic level, many SP-I terminals were seen closely associated with TH-I dendrites and somata. At the electron microscopic level, SP-I terminals synapsing on TH-I structures were also readily encountered. SP-I terminals contained small, clear, and predominantly spherical vesicles (32 +/- 4 nm diameter), as well as large dense-cored vesicles approximately 100 nm in diameter. Postsynaptic TH-I dendritic profiles of various calibers and somata were encountered. These postsynaptic TH-I structures often showed postsynaptic densities. The morphological features of the SP-TH synapses in the present study, that is, the size of synaptic vesicles and the presence of postsynaptic densities, are quite different from those of central carotid sinus afferent synapses reported in our previous study [Chen et al. (1992), J. Neurocytol., 21:137-147]. Therefore, most of the SP terminals of the SP-TH synapses in the NTScom appear not to originate from the carotid sinus afferents. SP-I second-order neurons of the carotid sinus afferent pathway [Chen et al. (1991), J. Auton. Nerv. Syst., 33:97-98] may be one of the possible sources of such terminals.

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Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

Cited by 19 publications

References 26 publications

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Carotid baroreceptor reflex coronary vasodilation in the dog.

Synaptic morphology of substance P terminals on catecholamine neurons in the commissural subnucleus of the nucleus tractus solitarii in the rat

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