Respiration 2 Flashcards
Explain how the pulmonary stretch receptors work
- Found in the upper airways
- Project via the vagus nerve to the NTS
- 2nd order neurons for this reflex are located in the NTS
- These afferents synapse onto neurons in the NTS that are GABergic (are inhibitory)
- These synapse onto inspiratory cells so that inspiration is reduced
- This will lead to a decrease in inspiratory time and frequency
Activation of PSRs leads to. . .
a termination of inspiration & a slowing of respiratory rhythm by ACTIVATION of post-I
- prolongation of expiration
- inhibition of inspiration
- slowing of respiratory rhythm
Identify the effects on the respiratory neurons following activation of PSRs to produce the response in breathing observed.
- excite post-inspiratory neurons
- inibit augmenting expiratory (or late E) neurons
- inhibit inspiratory neurons
- inhibit pre-inspiratory neurons
What is the Hering-Breuer Reflex?
- activated by pulmonary stretch receptors
- found in smooth muscle in lungs; slowly adapting receptors
When are pulmonary stretch receptors activated?
- either by electrical stimulation
- inflating lungs and holding it to a particular pressure
Increased sensory activity of the pulmonary-stretch lung afferents (via the vagus nerve) results in inhibition of the central inspiratory drive and thus inhibition of inspiration and initiation of expiration.
Blood vessels are surrounded by glomus cells (type I) & glial-like unsheathing cells (type II).
- When glomus cells detect hypoxia, this causes depolarization of cell membrane
- e.g. inhibiton of K+ channels which causes membrane depolarization
- This activates voltage-gated calcium channels
- Causes vesicular release of ATP (neurotransmitter)
- Released ATP activates P2X2 receptor
- This generates a depolarization at these afferents
- This increases the activity of these afferents up to 2nd order neurons
- At the same time, ATP binds to local P2Y receptors on the type II cells
- This also causes depolarization of type II cells which causes release of ATP
- This then perpetuates excitation within the system
P2X2 = ionotropic
P2Y receptors = GPCRs
Peripheral chemoreceptors are also sensitive to hypercapnia
High CO2 levels (along with low O2)
They are also sensitive to low pH in the blood
Central chemoreceptors respond to. . .
high CO2 in the cerebrospinal fluid
Glomus cells / type I cells in the carotid body respond to hypoxia and hypercapnia, and transmit their signal via paracrine actions to the . . .
glossopharyngeal nerve
Explain how peripheral chemoreceptors respond to changes in oxygen levels
There are two main areas - the carotid body (collection of cells) and the aortic body
Carotid bodies send afferents via glossopharyngeal nerve (IX) while the aortic bodies send them via the vagus nerve (X)
Both terminate in the NTS which is where the 2nd order neurons are
Some exit to the spinal cord & via symapthetic NS synapse onto the heart
Others exit via vagus nerve and synapse at the heart
What does an activation of central chemoreceptors do?
These chemoreceptors are believed to be found in the RTN (retrotrapezoid nucleus)
They lead to an INCREASE in respiration and an INCREASE in sympathetic activity
What happens if CO2 is too high in the blood?
H+ ions will activate:
VMS astrocytes, TASK-2 (ionotropic) & GPR4 (GPCR)
VMS astrocytes –> release ATP –> activates the RTN neuron -> increases breathing
TASK-2 & GPR4 -> activates RTN neuron –> increases breathing
GPR4 also –> inhibits K+ leak channels –> membrane potential increases