Chemical regulation of

respiration
By Anjana Saini
MBBS 1st Year Student
KIMS Koppal
CHEMICAL MECHANISM
Chemical mechanism of regulation of respiration is
operated through the chemoreceptors.
Chemoreceptors are the sensory nerve endings, which
give response to changes in chemical constituent of blood.

The two sets of chemoreceptors that detect these chemical

changes in blood are
 PERIPHERAL CHEMORECPTORS

Peripheral chemoreceptors are located in the Carotid and

Aortic Bodies.
They respond to changes in PO2, PCO2 and pH in arterial
blood.
Carotid and Aortic bodies send signals to the dorsal respiratory
group of neurons in medulla to increase ventilation
Most sensitive to PO2
Carotid Bodies
Small chemoreceptive organ located at the bifurcation of the common carotid
arteries
Afferent nerves from carotid bodies travel to the brain stem in the
glossopharyngeal nerve
Receive unusually high blood flow about 2L/100grm of tissue/min
They have high metabolic rate
Easily detect minor changes in PO2 PCO2 and pH
Consist of two types of cell Type1 and Type2
Aortic Bodies
Located along the ascending aorta and arch of the aorta

These are relatively less effective then carotid chemoreceptor

Sensitivity of chemoreceptor
The chemoreceptor respond to hypoxia, hypercapnia and acidosis

1. The sensor for chemical stimulus is the glomus cell

2. Inhibition of K+ channel result in depolarisation induced opening of voltage
gated calcium channel
3. The mechanism that cause inhibition of potassium channel by each stimulus
is different
 Hypoxia

Hypoxia is the major stimulus for activation of peripheral chemoreceptor

Decrease in PaO2 less than 100 mm-hg results in progressive increase in the firing
rate of afferent nerves that increase ventilation

Response is most effective at PO2 less than 60 mm-hg

Mechanism
Hypercapnia
rate of discharge of carotid and aortic chemoreceptors increase linearly with
increase in paco2. this directly increase the ventilatory response to carbon dioxide
The CO2 is produced by metabolism thus increase metabloism to stimulate
respiration which in return remove CO2 from the body ventilation remains elevated
till arterial pCO2 returns to normal
1. Increase in PaCO2 stimulates peripheral chemoreceptor by increasing CO2 in
glomus cell in fact H+ formed from H2CO3 from glomus cell is the actual
stimulates rather than molecular CO2
2. Hypoxia affects ventilation mainly by peripheral chemoreceptor whereas the
hypercapnia affects mainly by central chemoreceptor
Metabloic acidosis
Metabloic acidosis is caused due to accumulation of non volatile acid like lactic
acid and keto acid

1. In the initial phase hyperventilation occur by stimulation of the peripheral

chemoreceptor by H+
2. In later phase if acidosis persist for days csf bicarbonate concentration is
adjusted downwards and ultimately ventilation increase further due to
stimulation of central chemoreceptor