CHEMICAL REGULATION OF RESPIRATION.

The central chemoreceptors located on or near the ventral surface of the medulla cause an increase in ventilation in response to an increase in PacO2 and to a lesser extent to a decrease in arterial pH because the blood brain barrier is relatively impermeable to hydrogen ions.

The peripheral chemoreceptors in the carotid bodies cause an increase in ventilation in response to an increase in PacO2 a decrease in arterial pH, and a decrease in PaO2. Neither the central chemoreceptors nor the carotid bodies are stimulated by a decrease in arterial blood pressure or O2 content.

The primary direct stimulus for central chemoreceptors is increased Ir concentration in the CSF and brain interstitial fluid. (But the H+ conc. in the brain parallels the arterial PCO2 and not arterial H+ conc.)

• There are 2 types of chemoreceptors regulating ventilation: central chemoreceptors (located in brain stem, mainly medulla) and the peripheral chemoreceptors (aortic and carotid bodies).
• They regulate ventilation by resonding to increased arterial H+ conc., increased PaCO₂, and decreased Pa02.

• Thus the peripheral chemoreceptors are stimulated by hypoxia, hypercapnia, and acidemia to cause hyperventilation; whereas central chemoreceptors are stimulated only by hypercapnia.

Why the central chemoreceptors respond to blood PaCO2 and not to blood H+ cone?.

• Even though the central chemoreceptors are directly stimulated by H+ ions: the blood H+ ions are poorly permeable through the blood brain barrier and hence are not able to regulate ventilation through the central chemoreceptors. Whereas CO₂ is highly permeable to the blood brain barrier. It enters the brain, where it is hydrated to give rise to H+ and HCO₃^– ions. Now these H+ ions directly stimulate the central chemoreceptors to regulate the ventilation.
• So the central chemoreceptors respond to changes in H+ ions in the cerebrospinal fluid and brain interstial which are brought about by changes in arterial PaCO2.

Remember:

The link between metabolism and ventilation is CO₂ and not 02.

Central chemoreceptors are stimulated mainly by the ↑H+ concentration caused by increased pCO2 levels. Since H+ cannot easily cross the blood brain barrier, increase in the blood H+ concentration have little effect in stimulating central chemo receptors. Increase in blood p CO2 causes CO2 to diffuse the  blood brain barrier with ease where it reacts with water to form carbonic acid. This carbonic acid in turn dissociates into H+ and bicarbonate ions. This H+ ions then have a potent stimulatory effect on the central chemo receptors. This question asks about the changes in blood that stimulates the central chemo receptors. So the correct answer is ↑p CO2 levels as H+ concentration in blood has little effect in stimulating the central chemo receptors.

Ref: Textbook Of Medical Physiology By Khurana, Page 458

Ans.B i.e. Anemic hypoxia

Peripheral chemoreceptors located in the carotid artery and aorta which sense the changes in PaO2 below 60mm Hg, pH, PaCO2, and they respond to changes in dissolved oxygen (PaO2 ).

Histotoxic hypoxia with metabolic acidosis, which will lead to an increase in H+ concentration, which in turn will stimulate the peripheral chemoreceptors.

Hemorrhage that produces hypotension,  decreased blood flow to the chemoreceptors and consequent stagnant hypoxia of these organs leads to the stimulation of peripheral chemoreceptors.

In the case of anemic hypoxia, the oxygen content is low but dissolved oxygen is within normal limits, hence it does not stimulate peripheral chemoreceptors

A i.e. TPCO2

A i.e. TH⁺

B i.e. Hypocapnia

Ans. is ‘a’ i.e., Carotid body tumor

o Non-chromaffin (neuroendocrine) cells of paraganglioma are also called glomus cells.

Ans. is ‘a’ i.e., H⁺ in CSF

The primary direct stimulus for central chemoreceptors is increased H⁺ concentration in the CSF and brain interstitial fluid.

Central chemoreceptors

• These receptors are located in a chemosensitive area on the ventral surface of the medulla near the exit of the ninth and tenth cranial nerves. The primary stimulus for the central chemoreceptors is an increase in the hydrogen ion concentration. Stimulation of central chemoreceptors by increased hydrogen ion concentration leads to excitation of the respiratory neurons, thereby producing an increase in the rate and depth of respiration.
• Although the primary stimulus for central chemoreceptors is an increase in hydrogen ion concentration, in actual practice the physiological stimulus is an increase in PCO₂. The reason is that hydrogen ions cannot cross blood – brain barrier. Therefore, a change in the blood hydrogen ion concentration does not change the hydrogen ion concentration in the immediate vicinity of the chemosensitive neurons (i.e., in CSF and brain interstitial fluid). On the other hand, CO₂ being lipid soluble can easily cross blood brain barrier. It enters the brain, where it is hydrated to give rise to fr and HCO₂– ions. Now these H’ directly stimulate the central chemoreceptors.
• Thus, central chemoreceptors are directly stimulated by an increase in H⁺ concentration in CSF and brain inerstitial tissue, which is brought about by change in arterial PCO₂ (PaCO₂).

Ans. is ‘c’ i.e., Chemoreceptors 

• Arterial chemoreceptors consist of globular aggregations of chemoreceptive cells (glomus cells), and supportive cells, separated from one another by fibrous tissue septa.
• In these setpa and between glomus cells, numerous capillaries and nerve fibers are seen.
• The glomus cells have the structure of endocrine amine hormone secreting cells.