Oxygen Sensing in the Carotid Body: Ideas and Models

Abstract

The carotid body is able to respond to changes of the arterial PO₂ in a range between 100 Torr and 30 Torr with the chemoreceptor nervous discharge peaking at the low arterial PO₂ values (Lahiri & DeLaney, 1975). It is not the scope of this article to review and speculate on the main neurotransmitter which is released in hypoxia from type I cells to excite adjacent nerve endings, nor on the different biophysical properties of the type I cells to facilitate this transmitter release. However, it is the aim of this article to review and to speculate on the different possibilities as to how oxygen changes might be sensed in the carotid body tissue leading to a nervous response. There are three different views concerning the oxygen sensing mechanism in the carotid body that should be mentioned:

• 1.) The mitochondria are the site of the oxygen sensing, i.e. when the tissue PO₂ in the carotid body tissue approaches values close to the critical mitochondrial PO₂ (PO₂ < 1 Torr) the hypoxia-induced decrease of cellular ATP serves as a triggering signal.

• 2.) Cytochrome aa₃ of carotid body mitochondria has an unusually low affinity for oxygen (PO₂ > 90 Torr) and redox changes of this cytochrome dependent on PO₂ serve as a signal.

• 3.) Hemeproteins not involved in the energy producing process by the cytochromes of the mitochondrial respiratory chain undergo redox changes dependent on PO₂, inducing the nervous chemoreceptor response.