scholarly journals Inhibitory input from slowly adapting lung stretch receptors to retrotrapezoid nucleus chemoreceptors

2007 ◽  
Vol 580 (1) ◽  
pp. 285-300 ◽  
Author(s):  
Thiago S. Moreira ◽  
Ana C. Takakura ◽  
Eduardo Colombari ◽  
Gavin H. West ◽  
Patrice G. Guyenet
Keyword(s):  
Inhibitory Input ◽  
Retrotrapezoid Nucleus ◽  
Stretch Receptors ◽  
Lung Stretch

scholarly journals Inhibitory input from slowly‐adapting lung receptors (SARs) to retrotrapezoid nucleus (RTN) chemoreceptors.

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Ana Carolina Takakura ◽  
Thiago Santos Moreira ◽  
Eduardo Colombari ◽  
Patrice G Guyenet
Keyword(s):  
Inhibitory Input ◽  
Retrotrapezoid Nucleus

Acute cardiovascular response to isocapnic hypoxia. I. A mathematical model

2000 ◽  
Vol 279 (1) ◽  
pp. H149-H165 ◽  
Author(s):  
Mauro Ursino ◽  
Elisa Magosso
Keyword(s):  
Mathematical Model ◽  
Central Nervous System ◽  
Heart Rate ◽  
Blood Flow ◽  
Nervous System ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Stretch Receptors ◽  
The Central Nervous System ◽  
Lung Stretch

A mathematical model of the acute cardiovascular response to isocapnic hypoxia is presented. It includes a pulsating heart, the systemic and pulmonary circulation, a separate description of the vascular bed in organs with the higher metabolic need, and the local effect of O2 on these organs. Moreover, the model also includes the action of several reflex regulatory mechanisms: the peripheral chemoreceptors, the lung stretch receptors, the arterial baroreceptors, and the hypoxic response of the central nervous system. All parameters in the model are given in accordance with the physiological literature. The simulated overall response to a deep hypoxia (28 mmHg) agrees with the experimental data quite well, showing a biphasic pattern. The early phase (8–10 s), caused by activation of peripheral chemoreceptors, exhibits a moderate increase in mean systemic arterial pressure, a decrease in heart rate, a quite constant cardiac output, and a redistribution of blood flow to the organs with higher metabolic need at the expense of other organs. The later phase (20 s) is characterized by the activation of lung stretch receptors and by the central nervous system hypoxic response. During this phase, cardiac output and heart rate increase together, and blood flow is restored to normal levels also in organs with lower metabolic need. The model may be used to gain a deeper understanding of the role of each mechanism in the overall cardiovascular response to hypoxia.

Acute cardiovascular response to isocapnic hypoxia. II. Model validation

2000 ◽  
Vol 279 (1) ◽  
pp. H166-H175 ◽  
Author(s):  
Mauro Ursino ◽  
Elisa Magosso
Keyword(s):  
Cardiac Output ◽  
Cardiovascular Response ◽  
Systemic Arterial Pressure ◽  
Severe Hypoxia ◽  
Physiological Data ◽  
Hypoxic Response ◽  
Stretch Receptors ◽  
Lung Stretch ◽  
The Impact

The role of the different mechanisms involved in the cardiovascular response to hypoxia [chemoreceptors, baroreceptors, lung stretch receptors, and central nervous system (CNS) hypoxic response] is analyzed in different physiological conditions by means of a mathematical model. The results reveal the following: 1) The model is able to reproduce the cardiovascular response to hypoxia very well between 100 and 28 mmHg Po 2. 2) Sensitivity analysis of the impact of each individual mechanism underlines the role of the baroreflex in avoiding excessive derangement of systemic arterial pressure and cardiac output during severe hypoxia and suggests the existence of significant redundancy among the other regulatory factors. 3) Simulation of chronic sinoaortic denervation (i.e., simultaneous exclusion of baroreceptors, chemoreceptors, and lung stretch receptors) shows that the CNS hypoxic response alone is able to maintain quite normal cardiovascular adjustments to hypoxia; however, suppression of the CNS hypoxic response, as might occur during anesthesia, led to a significant arterial hypotension. 4) Simulations of experiments with controlled ventilation show a significant decrease in heart rate that can only partly be ascribed to inactivation of lung stretch receptors. 5) Simulations performed by maintaining constant cardiac output suggest that during severe hypoxia the chemoreflex can produce a significant decrease in systemic blood volume. In all the previous cases, model predictions exhibit a satisfactory agreement with physiological data.

Influence of Lung Stretch Receptors on the Cough Reflex in Rabbits

Respiration ◽  
1984 ◽  
Vol 45 (3) ◽  
pp. 161-168 ◽  
Author(s):  
J. Hanáček ◽  
A. Davies ◽  
J.G. Widdicombe
Keyword(s):  
Cough Reflex ◽  
Stretch Receptors ◽  
Lung Stretch

scholarly journals Somatostatin-expressing parafacial neurons are CO2/H+ sensitive and regulate baseline breathing

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Colin M Cleary ◽  
Brenda M Milla ◽  
Fu-Shan Kuo ◽  
Shaun James ◽  
William F Flynn ◽  
...  
Keyword(s):  
Neural Activity ◽  
Respiratory Activity ◽  
Control Of Breathing ◽  
Dravet Syndrome ◽  
Inhibitory Neurons ◽  
Inhibitory Input ◽  
Dependent Manner ◽  
Glutamatergic Neurons ◽  
Retrotrapezoid Nucleus ◽  
Synaptic Interactions

Glutamatergic neurons in the retrotrapezoid nucleus (RTN) function as respiratory chemoreceptors by regulating breathing in response to tissue CO2/H+. The RTN and greater parafacial region may also function as a chemosensing network composed of CO2/H+-sensitive excitatory and inhibitory synaptic interactions. In the context of disease, we showed that loss of inhibitory neural activity in a mouse model of Dravet syndrome disinhibited RTN chemoreceptors and destabilized breathing (Kuo et. al., 2019; 25). Despite this, contributions of parafacial inhibitory neurons to control of breathing are unknown, and synaptic properties of RTN neurons have not been characterized. Here, we show the parafacial region contains a limited diversity of inhibitory neurons including somatostatin (Sst)-, parvalbumin (Pvalb)- and cholecystokinin (Cck)-expressing neurons. Of these, Sst-expressing interneurons appear uniquely inhibited by CO2/H+. We also show RTN chemoreceptors receive inhibitory input that is withdrawn in a CO2/H+-dependent manner, and chemogenetic suppression of Sst+ parafacial neurons, but not Pvalb+ or Cck+ neurons, increases baseline breathing. These results suggest Sst-expressing parafacial neurons contribute to RTN chemoreception and respiratory activity.

Sign in / Sign up

Export Citation Format

Share Document