scholarly journals PreBötzinger complex neurons drive respiratory modulation of blood pressure and heart rate

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Clément Menuet ◽  
Angela A Connelly ◽  
Jaspreet K Bassi ◽  
Mariana R Melo ◽  
Sheng Le ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Respiratory Neurons ◽  
Neuron Activity ◽  
Neuronal Tracing ◽  
Cardiovascular Neurons ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

Heart rate and blood pressure oscillate in phase with respiratory activity. A component of these oscillations is generated centrally, with respiratory neurons entraining the activity of pre-sympathetic and parasympathetic cardiovascular neurons. Using a combination of optogenetic inhibition and excitation in vivo and in situ in rats, as well as neuronal tracing, we demonstrate that preBötzinger Complex (preBötC) neurons, which form the kernel for inspiratory rhythm generation, directly modulate cardiovascular activity. Specifically, inhibitory preBötC neurons modulate cardiac parasympathetic neuron activity whilst excitatory preBötC neurons modulate sympathetic vasomotor neuron activity, generating heart rate and blood pressure oscillations in phase with respiration. Our data reveal yet more functions entrained to the activity of the preBötC, with a role in generating cardiorespiratory oscillations. The findings have implications for cardiovascular pathologies, such as hypertension and heart failure, where respiratory entrainment of heart rate is diminished and respiratory entrainment of blood pressure exaggerated.

scholarly journals Author response: PreBötzinger complex neurons drive respiratory modulation of blood pressure and heart rate

2020 ◽  
Author(s):  
Clément Menuet ◽  
Angela A Connelly ◽  
Jaspreet K Bassi ◽  
Mariana R Melo ◽  
Sheng Le ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Author Response ◽  
Respiratory Modulation ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

scholarly journals Inspiratory Off-Switch Mediated by Optogenetic Activation of Inhibitory Neurons in the preBötzinger Complex In Vivo

2021 ◽  
Vol 22 (4) ◽  
pp. 2019
Author(s):  
Swen Hülsmann ◽  
Liya Hagos ◽  
Volker Eulenburg ◽  
Johannes Hirrlinger
Keyword(s):  
Respiratory Rate ◽  
Respiratory Rhythm ◽  
Inhibitory Neurons ◽  
Respiratory Neurons ◽  
Ventrolateral Medulla ◽  
Transgenic Mouse Line ◽  
Respiratory Network ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

The role of inhibitory neurons in the respiratory network is a matter of ongoing debate. Conflicting and contradicting results are manifold and the question whether inhibitory neurons are essential for the generation of the respiratory rhythm as such is controversial. Inhibitory neurons are required in pulmonary reflexes for adapting the activity of the central respiratory network to the status of the lung and it is hypothesized that glycinergic neurons mediate the inspiratory off-switch. Over the years, optogenetic tools have been developed that allow for cell-specific activation of subsets of neurons in vitro and in vivo. In this study, we aimed to identify the effect of activation of inhibitory neurons in vivo. Here, we used a conditional transgenic mouse line that expresses Channelrhodopsin 2 in inhibitory neurons. A 200 µm multimode optical fiber ferrule was implanted in adult mice using stereotaxic surgery, allowing us to stimulate inhibitory, respiratory neurons within the core excitatory network in the preBötzinger complex of the ventrolateral medulla. We show that, in anesthetized mice, activation of inhibitory neurons by blue light (470 nm) continuously or with stimulation frequencies above 10 Hz results in a significant reduction of the respiratory rate, in some cases leading to complete cessation of breathing. However, a lower stimulation frequency (4–5 Hz) could induce a significant increase in the respiratory rate. This phenomenon can be explained by the resetting of the respiratory cycle, since stimulation during inspiration shortened the associated breath and thereby increased the respiratory rate, while stimulation during the expiratory interval reduced the respiratory rate. Taken together, these results support the concept that activation of inhibitory neurons mediates phase-switching by inhibiting excitatory rhythmogenic neurons in the preBötzinger complex.

Cardiovascular Responding during Anger and Fear Imagery

1982 ◽  
Vol 50 (1) ◽  
pp. 219-230 ◽  
Author(s):  
Richard J. Roberts ◽  
Theodore C. Weerts
Keyword(s):  
College Students ◽  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Scene Change ◽  
Emotional Responding ◽  
Analysis Of Change ◽  
Screening Interview

This study was designed to determine if visualization of anger- and fear-provoking scenes produced differential physiological patterns similar to those produced by in vivo manipulations. Normotensive college students were selected on the basis of their responses to newly developed Anger and Fear/Anxiety questionnaires and for their ability to construct arousing scenes during a screening interview. In a 2 × 2 design (intensity × emotion), four scenes (high and low anger, high and low fear) were constructed individually for each of 16 subjects to imagine. Diastolic blood pressure, systolic blood pressure, and heart rate were monitored during visualization of each scene. Change in diastolic blood pressure was significantly greater for high anger than for high fear as predicted. Analysis of change in heart rate and systolic blood pressure showed significant effects for intensity only. These results provide further support for the concept of physiological differentiation in human emotion and suggest the utility of imagery for systematic study of human emotional responding.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Arteries ◽  
Neural Mechanism ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Anesthetized Dogs ◽  
Arterial Constriction ◽  
Synthase Inhibitor

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

Frequency-force relationships of mammalian ventricular muscle in vivo and in vitro

1976 ◽  
Vol 230 (3) ◽  
pp. 631-636 ◽  
Author(s):  
ML Kahn ◽  
F Kavaler ◽  
VJ Fisher
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Room Temperature ◽  
Physiological Role ◽  
Ventricular Muscle ◽  
Contractile State ◽  
Force Relationship

The change in contractility with increasing heart rate was studied in the left ventricle of dogs and in isolated trabeculae carneae of cats. For some of the studies in situ a transient isovolumic state was created by aortic occlusion. At physiological temperatures the frequency-force relationship is flatter than at room temperature and at the same temperature it is flatter in vivo than in vitro. The frequency-(dF/dt)max relationship is steeper than the frequency-force relationship at both temperatures in vivo and in vitro. The frequency-(dF/dt)max relationship is steeper in vitro than it is in situ, although the discrepancy is less marked than in the case of the frequency-force relationship. It is concluded that "staircase" plays less of a physiological role in adjustment of contractile state in situ than might be inferred from studies of isolated tissue.

scholarly journals Human neuropeptide Y potentiates α1-adrenergic blood pressure responses in vivo

1998 ◽  
Vol 275 (3) ◽  
pp. H760-H766 ◽  
Author(s):  
Leander V. Schuerch ◽  
Lilly M. Linder ◽  
Eric Grouzmann ◽  
Walter E. Haefeli
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Neuropeptide Y ◽  
Blood Pressure Response ◽  
Human Hand ◽  
Response Curves ◽  
Fourfold Increase ◽  
Dose Rates ◽  
Blood Pressure Responses

Human neuropeptide Y (hNPY) potentiates the postjunctional vasoconstrictor effects of α1-adrenoceptor agonists in animals and in human hand veins in vivo. We therefore hypothesized that such an interaction might also occur in the human arterial bed. With the present single-blind cross-over study in 12 healthy volunteers, the effect of subpressor doses of hNPY on the blood pressure response to α1-adrenoceptor stimulation was evaluated. Dose-response curves were constructed to intravenously infuse phenylephrine with and without coinfusion with two different doses of hNPY (1.4 and 14.3 pmol ⋅ kg−1 ⋅ min−1). Blood pressure, heart rate, and forearm blood flow were recorded, and plasma hNPY was determined. During infusion of the higher hNPY dose, which increased hNPY from 24.0 ± 12.0 to 495.1 ± 12.6 pmol/l, blood pressure curves were 2.4-fold shifted toward lower phenylephrine dose rates ( P < 0.001). Forearm vascular resistance showed a similar trend, whereas the counterregulatory decrease of heart rate was similar in both groups. In contrast, the lower hNPY dose rate producing a fourfold increase in hNPY concentrations did not modify the response to phenylephrine. This in vivo study in humans demonstrates that hNPY induced potentiating effects on α1-adrenergic constriction also in the systemic arterial circulation and suggests that circulating hNPY may participate in the control of vascular tone.

scholarly journals Defining preBötzinger Complex Rhythm- and Pattern-Generating Neural Microcircuits In Vivo

Neuron ◽  
2016 ◽  
Vol 91 (3) ◽  
pp. 602-614 ◽  
Author(s):  
Yan Cui ◽  
Kaiwen Kam ◽  
David Sherman ◽  
Wiktor A. Janczewski ◽  
Yu Zheng ◽  
...  
Keyword(s):  
Prebotzinger Complex ◽  
Prebötzinger Complex
Sign in / Sign up

Export Citation Format

Share Document