Effect of selective denervation of baroreceptors on pulmonary ventilation and arterial pressure lability in rat.

Mauad, Helder; Glass, Mogens L.; Machado, Benedito H.

doi:10.1161/01.hyp.19.2_suppl.ii182

Cited by 14 publications

(16 citation statements)

References 13 publications

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“…The relative contributions of aortic and carotid baroreceptors to AP regulation have been found to be different according to the animal model (Edis, 1971;Guo et al 1982;Mauad et al 1992;Thrasher & Shifflett, 2001). It has been suggested that aortic baroreceptors are more effective in controlling reflex heart rate (HR) responses in conscious dogs (Vatner et al 1970;Ito & Scher, 1978).…”

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confidence: 99%

Effect of baroreceptor denervation on the autonomic control of arterial pressure in conscious mice

Rodrigues

Oliveira

Salgado

et al. 2011

Experimental Physiology

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This study evaluated the role of arterial baroreceptors in arterial pressure (AP) and pulse interval (PI) regulation in conscious C57BL mice. Male animals, implanted with catheters in a femoral artery and a jugular vein, were submitted to sino-aortic (SAD), aortic (Ao-X) or carotid sinus denervation (Ca-X), 5 days prior to the experiments. After basal recording of AP, the lack of reflex bradycardia elicited by administration of phenylephrine was used to confirm the efficacy of SAD, and cardiac autonomic blockade with methylatropine and propranolol was performed. The AP and PI variability were calculated in the time and frequency domains (spectral analysis/fast Fourier transform) with the spectra quantified in low-(LF; 0.25-1 Hz) and high-frequency bands (HF; 1-5 Hz). Basal AP and AP variability were higher after SAD, Ao-X or Ca-X than in intact mice. Pulse interval was similar among the groups, whereas PI variability was lower after SAD. Atropine elicited a slight tachycardia in control mice but did not change PI after total or partial denervation. The bradycardia caused by propranolol was higher after SAD, Ao-X or Ca-X compared with intact mice. The increase in the variability of AP was accompanied by a marked increase in the LF and HF power of the AP spectra after baroreceptor denervation. The LF and HF power of the PI were reduced by SAD and by Ao-X or Ca-X. Therefore, both sino-aortic and partial baroreceptor denervation in mice elicits hypertension and a remarkable increase in AP variability and cardiac sympathetic tonus. Spectral analysis showed an important contribution of the baroreflex in the power of LF oscillations of the PI spectra. Both sets of baroreceptors seem to be equally important in the autonomic regulation of the cardiovascular system in mice.

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confidence: 99%

Effect of baroreceptor denervation on the autonomic control of arterial pressure in conscious mice

Rodrigues

Oliveira

Salgado

et al. 2011

Experimental Physiology

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“…In previous studies we observed that awake normal rats present deep breath events at regular intervals associated with oscillations in arterial blood pressure and heart rate (2,3). These studies also showed that in rats with sino-aortic deafferentation the deep breath events were consistently accompanied by substantial and abrupt reductions of arterial pressure, whereas this effect was markedly lower in intact rats.…”

Section: Introductionmentioning

confidence: 62%

“…The transition from REM sleep to wakefulness is also associated with a deep breath episode that seems to be a marker for the normalization of the frequency and tidal volume of the ventilatory cycle. The cardiovascular changes observed during the SWS desynchronization and simultaneous to the deep breaths were not greater probably because of the buffering role played by the arterial baroreceptors (2,3).…”

Section: Discussionmentioning

confidence: 92%

“…Deep breaths induce a 4-5-fold increase in tidal volume (2) and this large expansion of the chest wall may induce cardiovascular changes such as hypotension and tachycardia that may be counterbalanced by cardiovascular reflexes. We have reported that the fall in blood pressure of rats submitted to removal of the arterial baroreceptors was greater than in control rats (2,3). Thus, on the basis of a previous study (2), we may suggest two mechanisms to explain the fall in pressure during deep breaths: 1) activation of cardiopulmonary receptors in response to hemodynamic changes secondary to the large expansion of the chest wall and 2) interaction of neurons in the brain stem associated with the central neural control of the circulation and ventilation, considering that ventilatory and cardiovascular changes occurred at the same time.…”

Section: ∆ Dapmentioning

confidence: 94%

“…Immediately after the fall in arterial pressure we also observed (Figure 1) a secondary increase in pressure, which may be related to autonomic adjustments in response to arterial baroreceptor deactivation during the fall in pressure. In previous studies it was observed that rats with sino-aortic deafferentation present a greater fall in arterial pressure during the episodes of electrocortical SWS desynchronization (1) and during deep breaths in the awake state (3). These data, taken together, indicate that arterial barore-ceptor reflex integrity plays a key role in counterbalancing the cardiovascular oscillations during deep breaths and the present data suggest that during SWS desynchronization the sensitivity of the baroreflex may be reduced since the fall in pressure at that time was greater than in the awake state.…”

Section: ∆ Dapmentioning

confidence: 99%

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Cardiovascular and respiratory changes during slow-wave sleep in rats are associated with electrocorticogram desynchronization

Dias-dos-Santos

Machado

1997

Braz J Med Biol Res

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In awake rats a single recurrent larger tidal volume (deep breaths) occurs at regular intervals, followed by oscillations in arterial pressure and heart rate. In the present study we recorded the changes in blood pressure, heart rate and ventilation during the wakefulness-sleep cycle identified by electrocorticographic records in order to determine whether the deep breaths and cardiovascular oscillations were associated with changes in the electrocorticogram. During several episodes of slow-wave sleep (SWS) in 7 rats the deep breaths and oscillations in arterial pressure and heart rate were preceded by SWS desynchronization. The interval between deep breaths during SWS was 71 ± 4 s, the period between initial desynchronization and the generation of deep breaths was 3.98 ± 0.45 s and the duration of SWS desynchronization was 11 ± 0.65 s. Hypotension (-16 ± 1 mmHg) and tachycardia (+15 ± 5 bpm) were observed during deep breaths in the SWS state. These data indicate that the oscillations in arterial pressure and heart rate during SWS are associated with deep breaths, which in turn are preceded by desynchronization of the electrocorticogram in this state of sleep.

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The release of inhibitory amino acids in the hypothalamus is tonically modified by impulses from aortic baroreceptors as a consequence of blood pressure fluctuations

Singewald

Kouvelas

Chen

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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We investigated in conscious, freely moving rats whether the release of GABA, taurine and arginine in the hypothalamus is influenced by impulses originating from peripheral baroreceptors. The posterior hypothalamic nucleus was superfused with artificial cerebrospinal fluid through a push-push cannula and the release of amino acids was determined in the hypothalamic superfusate of control rats, as well as of rats after bilateral aortic denervation (AD). AD led to hypertension and increased the lability of arterial pressure. In sham-operated rats, intravenous infusion of phenylephrine increased blood pressure and the hypothalamic release of GABA and taurine. AD almost abolished the phenylephrine-induced release of the inhibitory amino acids. Similarly, the pressor response to hypervolaemia, elicited by blood injection, enhanced the release rates of GABA and taurine only in sham-operated rats. Baroreceptor unloading evoked either by intravenous infusion of nitroprusside, or by haemorrhage, decreased the release rates of GABA and taurine in sham-operated rats but not in AD rats. Electrical stimulation of the afferent aortic depressor nerve enhanced extracellular GABA and taurine in the posterior hypothalamic nucleus. The release rate of arginine was not influenced by alterations in baroreceptor activity either in sham-operated or in AD rats. The findings support the idea that, in the hypothalamus, GABA and taurine are involved in central blood pressure regulation. The release of these two amino acids seems to be driven tonically by baroreceptor impulses. Moreover, the findings indicate that the baroreceptors of the aortic arch play a crucial role in the mediation of changes in hypothalamic GABA and taurine outflow so as to counteract blood pressure fluctuations.

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Effect of selective denervation of baroreceptors on pulmonary ventilation and arterial pressure lability in rat.

Cited by 14 publications

References 13 publications

Effect of baroreceptor denervation on the autonomic control of arterial pressure in conscious mice

Effect of baroreceptor denervation on the autonomic control of arterial pressure in conscious mice

Cardiovascular and respiratory changes during slow-wave sleep in rats are associated with electrocorticogram desynchronization

The release of inhibitory amino acids in the hypothalamus is tonically modified by impulses from aortic baroreceptors as a consequence of blood pressure fluctuations

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