Abstract
The specialized oxygen-sensing tissues include the carotid body and arterial smooth muscle cells in the pulmonary artery (PA) and ductus arteriosus (DA). We discuss the evidence that changes in oxygen tension are sensed through changes in redox status " Redox" changes imply the giving or accepting of electrons. This might occur through the direct tunneling of electrons from mitochondria or redox couples to an effector protein (e.g. ion channel). Alternatively, the electron might be transferred through reactive oxygen species from mitochondria or an NADPH oxidase isoform. The PA's response to hypoxia and DA's response to normoxia result from reduction or oxidation, respectively. These opposing redox stimuli lead to K+ channel inhibition, membrane depolarization and an increase in cytosolic calcium and/or calcium sensitization that causes contraction. In the neuroendocrine cells (the type 1 cell of the carotid body, neuroepithelial body and adrenomedullary cells), the response is secretion. We examine the roles played by superoxide anion, hydrogen peroxide and the anti-oxidant enzymes in the signaling of oxygen tensions.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 182-191 |
| Number of pages | 10 |
| Journal | Respiratory Physiology and Neurobiology |
| Volume | 174 |
| Issue number | 3 |
| DOIs | |
| State | Published - Dec 31 2010 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work is supported by Veterans Administration Research funding, NIH-RO1-HL65322 , NIH-RO1-HL071115 and 1RC1HL099462-01 , the American Heart Association (AHA) and the Roche Foundation for Anemia Research .
Keywords
- Hypoxic pulmonary vasoconstriction
- Oxygen sensing
- Redox