Respiratory effects of brief baroreceptor stimuli in the anesthetized dog

Dove, E.L.; Katona, Péter

doi:10.1152/jappl.1985.59.4.1258

Cited by 18 publications

(11 citation statements)

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“…In their study, the authors showed convincing examples of both effects and noted that tidal volume was not significantly affected. Similar findings in the dog have been reported by other groups (Brunner et al 1982; Dove et al 1985). In contrast, using the same approach, Maass-Moreno and Katona lengthened TE but shortened TI in the cat (Maass-Moreno et al 1989).…”

Section: Discussionsupporting

confidence: 92%

“…Such effects may underlie the variability of respiratory responses (particularly pertaining to TI) reported in the literature. Baroreceptor activation has been reported to have bradypneic (Brunner et al 1982; Dove et al 1985) or no effects (Grunstein et al 1975; Miserocchi et al 1980) on respiratory frequency, and to either lengthen (Brunner et al 1982; Dove et al 1985) or shorten TI (Maass-Moreno et al 1989). …”

Section: Discussionmentioning

confidence: 99%

“…For example, Sapru and colleagues (1981) reported that in decerebrate non-vagotomized Wistar rats, aortic depressor nerve (ADN) stimulation completely arrests respiratory rhythm. In contrast, Miserocchi & Quinn (1980) found no effects of hemorrhagic hypotension on respiratory frequency in the cat, whereas Dove & Katona (1985) found that brief baroreceptor activation prolonged inspiratory (TI) and expiratory (TE) duration. Finally, Hayashi et al (1993) found no effect of aortic nerve stimulation on respiratory frequency in urethane-anaesthetised Sprague Dawley rats.…”

Section: Introductionmentioning

confidence: 94%

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Effects of baroreceptor activation on respiratory variability in rat

McMullan

Farnham

Pilowsky

2009

Respiratory Physiology & Neurobiology

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Controversy surrounds the respiratory responses to baroreceptor activation. Although many reflexes that effect respiration (e.g. chemoreflexes and nociceptive reflexes) frequently affect cardiovascular parameters, the effect of baroreflex stimulation within normal physiological limits is generally considered to affect only blood pressure and heart rate. Even though previous authors have reported that baroreceptor activation can affect respiratory activity, the effects on respiratory frequency and amplitude are highly variable, and changes in perfusion evoked by blood pressure manipulation could account for the observed effects. Here, we determined the respiratory effects of activating arterial baroreceptors by intravenous injection of phenylephrine or angiotensin II, or by electrical stimulation of the aortic depressor nerve (ADN). In urethane-anaesthetized vagotomized rats, 1, 2 and 4 second trains of tetanic ADN stimulation evoked 3.1 ± 1.1%, 11.2 ± 13.6% and 21.9 ± 8.9% increases in inspiratory (TI) time and 26.5 ± 18%, 23.4 ± 15.7% and 34.6 ± 20.9% increases in expiratory (TE) time respectively (P < 0.05 in both cases), but no effect on the amplitude of bursts recorded in the phrenic nerve. Similar effects were observed following pressor trials evoked by intravenous PE (TE: +26.1 ± 9.1%, P<0.01), but not Ang II. Intermittent ADN stimulation (single pulse, 1 Hz) significantly increased the variability of TI during periods of low respiratory drive (P < 0.05) without significantly affecting any other parameters. We propose that a specific baroreceptor-respiratory response exists that is independent of changes in blood flow. In contrast to the effects of baroreceptor stimulation on sympathetic nerve activity, the baro-respiratory response is subtle and highly dependent on respiratory drive.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

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Effects of baroreceptor activation on respiratory variability in rat

McMullan

Farnham

Pilowsky

2009

Respiratory Physiology & Neurobiology

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“…Our data provide a neural substrate for the expiratory– facilitatory response to activation of baroreceptors (Brunner et al, 1982; Dove and Katona, 1985; Grunstein et al, 1975; Li et al, 1999a,b; Lindsey et al, 1998; Nishino and Honda, 1982; Richter and Seller, 1975; Speck and Webber, 1983; Stella et al, 2001). We clearly demonstrate that barostimulation activates post-I neurones and depresses aug-E neurones.…”

Section: Discussionmentioning

confidence: 76%

Effect of baroreceptor stimulation on the respiratory pattern: Insights into respiratory–sympathetic interactions

Baekey

Molkov

Paton

et al. 2010

Respiratory Physiology & Neurobiology

143

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Sympathetic nerve activity (SNA) is modulated by respiratory activity which indicates the existence of direct interactions between the respiratory and sympathetic networks within the brainstem. Our experimental studies reveal that TE prolongation evoked by baroreceptor stimulation varies with respiratory phase and depends on the pons. We speculate that the sympathetic baroreceptor reflex, providing negative feedback from baroreceptors to the rostral ventrolateral medulla and SNA, has two pathways: one direct and independent of the respiratory–sympathetic interactions and the other operating via the respiratory pattern generator and is hence dependent on the respiratory modulation of SNA. Our experimental studies in the perfused in situ rat preparation and complementary computational modelling studies support the hypothesis that baroreceptor activation during expiration prolongs the TE via transient activation of post-inspiratory and inhibition of augmenting expiratory neurones of the Bötzinger Complex (BötC). We propose that these BötC neurones are also involved in the respiratory modulation of SNA, and contribute to the respiratory modulation of the sympathetic baroreceptor reflex.

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“…The unified model defines a neural substrate for the expiratory-facilitatory response to activation of baroreceptors (Brunner et al, 1982; Dove and Katona, 1985; Grunstein et al, 1975; Li et al, 1999a,b; Lindsey et al, 1998; Nishino and Honda, 1982; Richter and Seller, 1975; Speck and Webber, 1983; Stella et al, 2001) and explains previous experimental findings that respiratory neurons, preferentially expiratory neurons, are modulated with the arterial pulse (Dick and Morris, 2004; Dick et al, 2005). This substrate can be used for further extending the model to incorporate interactions with the parasympathetic nervous system, since baroactivated post-I neurons were also found to be crucially involved in the modulation of cardiac vagal motoneurons (Gilbey et al, 1984).…”

Section: Unified Theoretical Framework For Respiratory–sympathetic mentioning

confidence: 75%

Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system

Molkov¹,

Zoccal²,

Baekey³

et al. 2014

Progress in Brain Research

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Respiratory modulation seen in the sympathetic nerve activity (SNA) implies that the respiratory and sympathetic networks interact. During hypertension elicited by chronic intermittent hypoxia (CIH), the SNA displays an enhanced respiratory modulation reflecting strengthened interactions between the networks. In this chapter, we review a series of experimental and modeling studies that help elucidate possible mechanisms of sympatho-respiratory coupling. We conclude that this coupling significantly contributes to both the sympathetic baroreflex and the augmented sympathetic activity after exposure to CIH. This conclusion is based on the following findings. (1) Baroreceptor activation results in perturbation of the respiratory pattern via transient activation of postinspiratory neurons in the Bötzinger complex (BötC). The same BötC neurons are involved in the respiratory modulation of SNA, and hence provide an additional pathway for the sympathetic baroreflex. (2) Under hypercapnia, phasic activation of abdominal motor nerves (AbN) is accompanied by synchronous discharges in SNA due to the common source of this rhythmic activity in the retrotrapezoid nucleus (RTN). CIH conditioning increases the CO2 sensitivity of central chemoreceptors in the RTN which results in the emergence of AbN and SNA discharges under normocapnic conditions similar to those observed during hypercapnia in naïve animals. Thus, respiratory–sympathetic interactions play an important role in defining sympathetic output and significantly contribute to the sympathetic activity and hypertension under certain physiological or pathophysiological conditions, and the theoretical framework presented may be instrumental in understanding of malfunctioning control of sympathetic activity in a variety of disease states.

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Respiratory effects of brief baroreceptor stimuli in the anesthetized dog

Cited by 18 publications

References 0 publications

Effects of baroreceptor activation on respiratory variability in rat

Effects of baroreceptor activation on respiratory variability in rat

Effect of baroreceptor stimulation on the respiratory pattern: Insights into respiratory–sympathetic interactions

Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system

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