An investigation into the physiological relevance of the vagal tachycardia in the anaesthetized dog

Markos, F.; Snow, H. M.

doi:10.1111/j.1748-1716.2006.01524.x

Cited by 4 publications

(4 citation statements)

References 16 publications

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“…The tachycardia was attenuated and not abolished completely by addition of a VIP antagonist, this result is similar to previous investigations using other VIP antagonists (Hill et al 1995). The physiological relevance and signiWcance of a tachycardia that can only be obtained, and has only been demonstrated experimentally, in the presence of atropine is questionable (Markos and Snow 2006). However, the relevance of the vagal tachycardia does not necessarily mean that VIP does not play a role in the vagal regulation of cardiac function.…”

Section: Discussionsupporting

confidence: 85%

Vagal postganglionic origin of vasoactive intestinal polypeptide (VIP) mediating the vagal tachycardia

Markos

Snow

2006

Eur J Appl Physiol

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Our aim was to confirm the role of postganglionic vagal fibres and vasoactive intestinal polypeptide (VIP) in mediating the vagal tachycardia in anaesthetised dogs. Vagal postganglionic stimulation after atenolol (1 mg/kg) and hexamethonium (10 mg/kg) caused a bradycardia (40 beats/min, n = 2), after atropine (0.5 mg/kg i.v.) the resulting tachycardia (37 beats/min) was attenuated by VIP receptor antagonism with VIP (6-28) (100 mug i.c.) by approximately 50%. VIP release from vagal postganglionic fibres mediates the vagal tachycardia.

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Section: Discussionsupporting

confidence: 85%

Vagal postganglionic origin of vasoactive intestinal polypeptide (VIP) mediating the vagal tachycardia

Markos

Snow

2006

Eur J Appl Physiol

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“…This may be observed as a ‘rebound’ tachycardia after vagal stimulation 23 or as an emergent tachycardia when the inhibitory action of the vagus is blocked by atropine 24 . Its physiological significance is dubious 25 15,26,27 .…”

Section: Introductionmentioning

confidence: 99%

“…24 Its physiological significance is dubious. 25 ) The negative inotropic action of the vagus is relatively weak. 15,26,27 Circulating adrenal catecholamines may reinforce the sympathetic influences on cardiac function.…”

Section: Introductionmentioning

confidence: 99%

Differential Control of Cardiac Functions by the Brain

Salo

Campos

McAllen

2006

Clin Exp Pharma Physio

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1. The idea is introduced that cardiac rate, contractility or atrioventricular (A-V) conduction spread may be controlled independently by the brain. Limited data from reflex studies are cited to support this view. 2. Evidence is presented that individual autonomic post- and preganglionic neurons have quite specific actions on the heart. Premotor and other central neurons can have preferential actions on heart rate, contractility or A-V conduction. 3. The functional implications of selective cardiac control are discussed.

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“…It is now generally accepted that VIP is the most likely mediator of the classical vagal tachycardia that occurs in response to high-frequency vagal stimulation in the presence of atropine (Hill et al 1995). However, the VIP-mediated vagal tachycardia cannot be obtained in the absence of muscarinic receptor antagonism and only increases heart rate significantly in response to a very high level of vagal activity, which strongly suggests that the vagal tachycardia is probably not physiologically relevant (Markos & Snow, 2006). It is more likely that the physiological function of VIP in the heart is not primarily related to its ability to increase heart rate by a direct action on the sinus node.…”

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confidence: 99%

Vasoactive intestinal polypeptide receptor antagonism enhances the vagally induced increase in cardiac interval of the rat atriumin vitro

Hogan

Markos

2006

Experimental Physiology

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The effect of vasoactive intestinal polypeptide (VIP) receptor antagonism on preganglionic vagal electrical stimulation and on vagal postganglionic activation using nicotine and 1,1-dimethyl-4-phenylpiperazinium iodide on cardiac interval was evaluated in the isolated innervated rat right atrium. The vagus was stimulated at 4, 8, 16 and 32 Hz, pulse duration 1 ms, 20 V, for 30 s. All experiments were carried out in the presence of atenolol (4 μM). Vagal stimulation caused a frequency-dependent increase in cardiac interval which was amplified significantly at each frequency, except at 32 Hz, following application of the VIP receptor antagonist VIP(6-28) at 2 nM in 15 rats. Application of the ganglionic antagonist hexmethonium (28 μM, n = 7 rats) prior to 2 nM VIP(6-28) abolished this effect. Increasing the concentration of VIP(6-28) 10-fold to 20 nM did not result in a greater increase in cardiac interval than that obtained at 2 nM. Nicotine (0.1, 0.3, 0.5, 1.0 and 2.0 mM) increased cardiac interval by direct activation of postganglionic vagal fibres, but 2 nM VIP(6-28) did not affect the nicotine concentration response (n = 6 rats). 1,1-Dimethyl-4-phenylpiperazinium iodide (25, 50, 100 and 200 μM; n = 6 rats) was also used to induce an increase in cardiac interval; again it was not significantly altered by 2 nM VIP(6-28). Therefore, VIP receptor antagonism enhances the magnitude of vagally induced cardiac slowing, probably via an action at the preganglionic-postganglionic synapse.

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An investigation into the physiological relevance of the vagal tachycardia in the anaesthetized dog

Abstract: The vagal tachycardia cannot be elicited without atropine suggesting that it does not play a significant physiological role.

Cited by 4 publications

References 16 publications

Vagal postganglionic origin of vasoactive intestinal polypeptide (VIP) mediating the vagal tachycardia

Vagal postganglionic origin of vasoactive intestinal polypeptide (VIP) mediating the vagal tachycardia

Differential Control of Cardiac Functions by the Brain

Vasoactive intestinal polypeptide receptor antagonism enhances the vagally induced increase in cardiac interval of the rat atriumin vitro

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