The actions of myelinated and non-myelinated vagal fibres on atrial contraction in the rabbit

McWilliam, P. N.; Woolley, Dean C.

doi:10.1016/0165-1838(88)90155-5

Cited by 7 publications

(8 citation statements)

References 10 publications

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“…The present experiments have demonstrated that in cats stimulation of non-myelinated vagal fibres can evoke falls in heart rate and confirms the work of others for rat and rabbit (Nosaka et al 1979;Wooley et al 1987). The relative efficacy of the species' cardiac C fibres depends on the method of analysis.…”

Section: Discussionsupporting

confidence: 77%

“…4B), whether the responses were expressed either as changes in heart rate or as cardiac interval. Evidence for a possible role for non-myelinated fibres in heart rate control has been provided previously in other species, such as rat (Nosaka et al 1979), rabbit (Heinbecker & Bishop, 1935;Wooley et at. 1987) and guinea-pig (McWilliam & Wooley, 1987).…”

Section: Discussionmentioning

confidence: 94%

“…Due to the remaining doubt, the experimental arrangement of Fig. 1 C does In all the species studied the chronotropic effects of both B-and C-fibre responses are blocked by the muscarinic receptor antagonist, atropine; but there are reports in rabbits that the bradycardia evoked by non-myelinated vagal axons is resistant to the nicotinic ganglion blocker, hexamethonium (Ford & McWilliam, 1986;Wooley et al 1987;McWilliam & Wooley, 1990 Burnstock, 1990), rats (Selyanko & Skok, 1992) and dogs (Xi-Moy, Randall & Wurster, 1993) is mediated by both fast and slow EPSPs which act via nicotinic and muscarinic Ml receptors, respectively. Using the techniques described in the present paper, preliminary studies have confirmed that in rabbits the bradycardia evoked by selectively stimulating non-myelinated vagal fibres is resistant to the nicotinic ganglion blockers hexamethonium and chlorisondamine but can be attenuated by low doses of pirenzipine, an antagonist at muscarinic Ml receptors (Jones & Jordan, 1993).…”

Section: Discussionmentioning

confidence: 99%

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Heart rate responses to selective stimulation of cardiac vagal C fibres in anaesthetized cats, rats and rabbits.

Jones

Wang

Jordan

1995

The Journal of Physiology

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1. The contribution of cardiac vagal C fibres to vagal chronotropic control in anaesthetized cats, rats and rabbits was analysed using electrical stimulation of the vagus nerve with a selective anodal block technique. 2. After bilateral vagotomy and pretreatment with atenolol, 10 Hz continuous selective stimulation of unmyelinated fibres in the cut peripheral end of the cervical vagus evoked a bradyeardia in anaesthetized rats, cats and rabbits. With this stimulation protocol the three species exhibited a similar lengthening of the heart period (R-R interval) when expressed as a percentage of their basal cardiac interval. 3. The mechanism of action of the selective blocking technique was analysed by recording eighty-nine single A-(n = 12), B-(n = 22) and C-fibre (n = 55) vagal-projecting neurones in the medulla of the rat. This demonstrated that the technique can selectively block conduction in myelinated fibres and that 'break excitation' is seen mainly in unmyelinated fibres. Although thirty C fibres showed break excitation sixteen did not and this difference could not be correlated with their axonal conduction velocity, chronaxie or initial segment frequency following. 4. Using the anodal block technique the vagal effects on heart rate were reanalysed in the cat by incorporating a collision technique. B fibres were activated orthodromically to evoke cardioinhibition and simultaneously antidromically to collide with errant B-fibre spikes activated at the electrode producing anodal block. With this protocol it was noted that the B-and C-fibre bradycardias were not additive. Using a double anodal block and collision technique, it was demonstrated that this phenomenon was likely to be due to occlusion of the effects of B and C fibres. 5. In conclusion, in addition to the well-defined effects of vagal B fibres on heart rate, selective stimulation of vagal C fibres also had a cardioinhibitory effect in all three species studied. However, since the effects of cardiac C fibres on heart rate was small, these neurones alone cannot account for the cardioinhibition of the pulmonary chemoreflex. It is likely that activation of both B-and C-fibre cardiac vagal preganglionic neurones accounts for this reflex cardioinhibition.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Heart rate responses to selective stimulation of cardiac vagal C fibres in anaesthetized cats, rats and rabbits.

Jones

Wang

Jordan

1995

The Journal of Physiology

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“…Therefore, the rate at which the arterial baroreflex resets may be the key to identifying the specific afferent population involved in this process. Perhaps the most convincing evidence for involvement of mechanosensitive afferents was reported by McWilliam and colleagues (McWilliam & Woolley, 1988; McWilliam et al 1991; McMahon & McWilliam, 1992). They found that very brief somatic stimulation (2–4 s) was sufficient to alter baroreflex function.…”

Section: Neural Feedback From Skeletal Muscle Modulates Arterial Baromentioning

confidence: 82%

Inhibitory neurotransmission in the nucleus tractus solitarii: implications for baroreflex resetting during exercise

Potts

2005

Experimental Physiology

130

121

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Inhibitory neurotransmission plays a crucial role in the processing of sensory afferent signals in the nucleus of the solitary tract (NTS). The aim of this review is to provide a critical overview of inhibitory mechanisms that may be responsible for altering arterial baroreflex function during physical activity or exercise. Over a decade ago, the view of reflex control of cardiovascular function during exercise was revised because of the finding that the arterial baroreflex is reset in humans, enabling continuous beat-to-beat reflex regulation of blood pressure and heart rate. During the ensuing decade, many investigators proposed that resetting was mediated by central neural mechanisms that were intrinsic to the brain. Recent experimental data suggest that rapid and reversible changes in γ-aminobutyric acid (GABA) inhibitory neurotransmission within the NTS play a fundamental role in this process. The hypothesis will be presented that baroreflex resetting by somatosensory input is mediated by: (1) selective inhibition of barosensitive NTS neurones; and (2) excitation of sympathoexcitatory neurones in the rostral ventrolateral medulla. Current research findings will be discussed that support an interaction between GABA and substance P (SP) signalling mechanisms in the NTS. An understanding of these mechanisms may prove to be essential for future detailed analysis of the cellular and molecular mechanisms underlying sensory integration in the NTS.

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“…Depending on animal species, myelinated only or both types of efferent vagal fibres reduce the heart rate and atrial contractility (e.g. Ford & McWilliam, 1986;McWilliam & Woolley, 1988). These effects of myelinated and non-myelinated fibres involve muscarinic receptors, but differ in the mechanisms involved.…”

Section: Humoral Mechanismsmentioning

confidence: 99%

Reflex effects on the coronary circulation

Mary

1992

Experimental Physiology

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The actions of myelinated and non-myelinated vagal fibres on atrial contraction in the rabbit

Cited by 7 publications

References 10 publications

Heart rate responses to selective stimulation of cardiac vagal C fibres in anaesthetized cats, rats and rabbits.

Heart rate responses to selective stimulation of cardiac vagal C fibres in anaesthetized cats, rats and rabbits.

Inhibitory neurotransmission in the nucleus tractus solitarii: implications for baroreflex resetting during exercise

Reflex effects on the coronary circulation

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