Tissue PO2 and mitochondrial enzymes. Cytochrome C oxidase as O2 sensor.

Abstract

The carotid body senses both oxygen and carbon dioxide, responding to either decreasing oxygen pressure or increasing carbon dioxide pressure with increasing afferent activity (for review see Lahiri, 1994; Gonzles et al. 1994). Although the afferent electrical activity indicates some interaction between the two sensory systems, the sensors themselves are independent (Mulligan and Lahiri, 1982). The afferent neural activity of the carotid body responds rapidly and precisely to alterations in the oxygen pressure of the blood in the carotid artery. This afferent neural activity increases many fold as the oxygen pressure in the carotid artery falls from about 100 mm Hg to about 30 mm Hg. The general problem of how the levels of nutrients, such as oxygen, in tissues is measured (sensed) and how that information is used to generate the appropriate physiological adjustment remain incompletely understood. In principle, a cell must measure the metabolite through a biochemical component that interacts in a concentration dependent manner. This interaction must then be communicated to the appropriate cellular response element via an intermediate signaling system. There have been several competing hypotheses concerning the identity of the oxygen sensor. These include mitochondrial oxidative phosphorylation (see Mulligan et al. 1981; Biscoe and Duchen, 1990), an oxygen sensitive ion channel (see Donnelly, 1999), a plasma membrane NADH oxidase (Acker and Xue, 1995). The idea that mitochondrial oxidative phosphorylation is responsible for oxygen sensing in the carotid