Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs.

Revington, Maureen; McCloskey, D.I.

doi:10.1113/jphysiol.1990.sp018216

Cited by 34 publications

(11 citation statements)

References 29 publications

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“…Neuropeptide Y released from sympathetic nerve terminals also interacts with ACh [8,11,47,48]. Conversely, the release of neuropeptide Y is prevented by simultaneous vagal stimulation [9,24]. As these studies have demonstrated mutually inhibitory prejunctional interactions, the phenomenon of bidirectional augmentation of dynamic heart rate regulation could not be directly explained.…”

Section: Prejunctional Mechanism Of Vago-sympathetic Interactionmentioning

confidence: 84%

Dynamic nonlinear vago-sympathetic interaction in regulating heart rate

1998

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Although the characteristics of the static interactions between the sympathetic and parasympathetic nervous systems in regulating heart rate have been well established, how the dynamic interaction modulates the heart rate response remains unknown. Thus, we investigated the dynamic interaction by estimating the transfer function from nerve stimulation to heart rate, using band-limited Gaussian white noise, in anesthetized rabbits. Concomitant tonic vagal stimulation at 5 and 10 Hz increased the gain of the transfer function relating dynamic sympathetic stimulation to heart rate by 55.0%+/-40.1% and 80.7%+/-50.5%, respectively (P < 0.05). Concomitant tonic sympathetic stimulation at 5 and 10 Hz increased the gain of the transfer function relating dynamic vagal stimulation to heart rate by 18.2%+/-17.9% and 24.1%+/-18.0%, respectively (P < 0.05). Such bidirectional augmentation was also observed during simultaneous dynamic stimulation of the sympathetic and vagal nerves independent of their stimulation patterns. Because of these characteristics, changes in sympathetic or vagal tone alone can alter the dynamic heart rate response to stimulation of the other nerve. We explained this phenomenon by assuming a sigmoidal static relationship between autonomic nerve activity and heart rate. To confirm this assumption, we identified the static and dynamic characteristics of heart rate regulation by a neural network analysis, using large-amplitude Gaussian white noise input. To examine the mechanism involved in the bidirectional augmentation, we increased cytosolic adenosine 3',5'-cyclic monophosphate (cAMP) at the postjunctional effector site by applying pharmacological interventions. The cAMP accumulation increased the gain of the transfer function relating dynamic vagal stimulation to heart rate. Thus, accumulation of cAMP contributes, at least in part, to the sympathetic augmentation of the dynamic vagal control of heart rate.

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Section: Prejunctional Mechanism Of Vago-sympathetic Interactionmentioning

confidence: 84%

Dynamic nonlinear vago-sympathetic interaction in regulating heart rate

1998

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“…The complex patterns of co-localisation of NPY with other neurochemicals in intrinsic, nonsympathetic neurones in the heart, as well as in sympathetic nerves of extrinsic origin, serve as a basis for the various interactions and neuromodulatory roles of NPY at several, pre-and postjunctional sites in the heart (e.g. Potter 1987; Revington and McCloskey 1990;Gulbenkian et al 1992;Armour et al 1993;Rubino et al 1996). In addition, our observation of the close apposition of NPY-immunoreactive and non-immunoreactive varicosities in nerve bundles may represent sites of prejunctional modulation by NPY of the activity of neurones that do not contain NPY (see Gulbenkian et al 1992;Rubino et al 1996).…”

Section: Discussionmentioning

confidence: 98%

“…Intracardiac neurones are sensitive to NPY (Armour et al 1993), and so the presence of NPY-immunoreactive nerve profiles associated with these intrinsic neurones in ganglia may indicate that this is the site for postjunctional interactions between the sympathetic and parasympathetic innervation of the heart that are mediated by NPY (e.g. Potter 1987;Revington and McCloskey 1990). Another possibility is that the NPY-immunoreactive nerve profiles seen in the ganglia are the terminals of other intrinsic, intracardiac interneurones and therefore NPY may be involved in local neuronal reflexes (Ardell et al 1991;Saffrey et al 1992;Allen et al 1994;Murphy et al 1994a, b).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y-immunoreactive intracardiac neurones, granule-containing cells and nerves associated with ganglia and blood vessels in rat and guinea-pig heart

Sosunov

Hassall

Loesch

et al. 1997

Cell and Tissue Research

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Intrinsic neuropeptide Y-containing neurones in rat and guinea-pig hearts were studied at the ultrastructural level by the pre-embedding peroxidase-antiperoxidase immunocytochemical technique. Intracardiac neuronal cell bodies were often weakly or moderately immunostained, and the labelling was usually pronounced in the Golgi complex, multivesicular bodies, some cisterns of granular endoplasmic reticulum and large granular vesicles. Neuropeptide Y-immunoreactive nerve fibres were also observed in association with intracardiac neurones. A subpopulation of neuropeptide Y-immunoreactive granule-containing cells in the rat heart are described for the first time and were very heavily labelled; other granule-containing cells were non-immunoreactive, but were contacted by neuropeptide Y-containing nerves. Preterminal regions of nerve fibres that were located in nerve bundles were only weakly neuropeptide Y-immunoreactive, in contrast to the heavy labelling observed in varicosities that contained many synaptic vesicles. Many neuropeptide Y-immunoreactive nerve fibres were associated with the coronary vasculature and were particularly prominent in the walls of small arteries and arterioles where labelled nerve varicosities were present close to the smooth muscle cells. Immunoreactive nerves were also seen in the myocardium, usually near to capillaries. In axonal varicosities, the central core of large granular vesicles was immunolabelled, and electron-dense immunoreactive material outlined the membranes of small and large clear vesicles. The significance of neuropeptide Y-immunoreactive intracardiac neurones and granule-containing cells and the origin of associated labelled nerve fibres in the heart are discussed.

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“…[6][7][8][9] With regard to the neural control of the heart, a number of studies have shown that an antecedent period of intense sympathetic stimulation can profoundly and persistently attenuate the chronotropic responses to subsequent vagal test stimulations.10-16 This profound inhibition of vagal efficacy by antecedent sympathetic activity is believed to be mediated by the release of a specific neuropeptide from the sympathetic nerve endings; in the dog, the specific neuromodulator is neuropeptide Y (NPY). [10][11][12][13][14][15][16] When intense vagal stimulation is given concurrently with the sympathetic stimulation, however, the chronotropic responses to subsequent vagal test stimulations are no longer attenuated. 15 Thus, a period of intense sympathetic activity alone would be expected to abolish or attenuate vagal preponderance for a substantial time after cessation of the antecedent sympathetic activity.…”

Section: Sequence Of Excitation As a Factor Inmentioning

confidence: 95%

“…[10][11][12][13][14][15][16] When intense vagal stimulation is given concurrently with the sympathetic stimulation, however, the chronotropic responses to subsequent vagal test stimulations are no longer attenuated. 15 Thus, a period of intense sympathetic activity alone would be expected to abolish or attenuate vagal preponderance for a substantial time after cessation of the antecedent sympathetic activity. Conversely, an equivalent period of concurrent intense vagal and sympathetic activity would be expected to have only a negligible influence on subsequent vagal preponderance.…”

Section: Sequence Of Excitation As a Factor Inmentioning

confidence: 95%

Sequence of excitation as a factor in sympathetic-parasympathetic interactions in the heart.

Yang

Levy

1992

Circulation Research

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We determined the influence of differences in the time of initiation of sympathetic and vagal stimulation (both at 10 Hz) on the cardiac autonomic interactions in 16 open-chest anesthetized dogs. We always ended the concurrent sympathetic and vagal stimulations simultaneously. Sympathetic stimulation alone for 1 minute increased heart rate by 90 +/- 7 (mean +/- SEM) beats per minute, and vagal stimulation alone for 1 minute decreased heart rate by 67 +/- 5 beats per minute; i.e., the algebraic sum of these responses was an increase of 23 beats per minute. However, combined sympathetic and vagal stimulation for 1 minute actually decreased heart rate by 35 beats per minute; i.e., the vagal effects predominated. When vagal stimulation was initiated first, the chronotropic responses to combined stimulation were not significantly affected by the duration of antecedent vagal stimulation. However, when sympathetic stimulation was initiated first, the vagal predominance (disparity between the summated individual responses and the combined response) progressively diminished as we increased the duration of antecedent sympathetic stimulation. The vagal predominance diminished from a value of 67 +/- 21 beats per minute when the stimulations were initiated simultaneously to a value of 37 +/- 21 beats per minute when the duration of antecedent sympathetic stimulation was 10 minutes. Sympathetic stimulation releases not only norepinephrine but also neuropeptide Y, and this neuropeptide inhibits vagal neurotransmission. Our data suggest, therefore, that the longer the antecedent sympathetic stimulation, the greater the inhibition of vagal neurotransmission (presumably by the neuropeptide Y) and, therefore, the less pronounced the vagal predominance.

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Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs.

Cited by 34 publications

References 29 publications

Dynamic nonlinear vago-sympathetic interaction in regulating heart rate

Dynamic nonlinear vago-sympathetic interaction in regulating heart rate

Neuropeptide Y-immunoreactive intracardiac neurones, granule-containing cells and nerves associated with ganglia and blood vessels in rat and guinea-pig heart

Sequence of excitation as a factor in sympathetic-parasympathetic interactions in the heart.

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