| First Author | Kazemian P | Year | 2001 |
| Journal | Respir Physiol | Volume | 126 |
| Issue | 2 | Pages | 89-101 |
| PubMed ID | 11348637 | Mgi Jnum | J:106249 |
| Mgi Id | MGI:3617933 | Doi | 10.1016/s0034-5687(01)00205-5 |
| Citation | Kazemian P, et al. (2001) Respiratory control in neonatal mice with NADPH oxidase deficiency. Respir Physiol 126(2):89-101 |
| abstractText | A membrane bound cytochrome b(558) (NADPH oxidase) is a candidate for the oxygen sensor in pulmonary neuroepithelial bodies (NEBs) - putative airway chemoreceptors. Recent electrophysiological studies on NEB from mice with NADPH oxidase deficiency (OD; gp(91phox) knock-out) have shown lack of response of O(2) sensitive K(+) current to hypoxia challenge compared with wild-type (WT) control mice. To assess the effects of oxidase deficiency on the control of ventilation at the whole animal level, respiratory measurements were conducted under normoxic and hypoxic conditions in neonatal OD mice and compared that with the WT control group. Five-day-old OD mice were faster and shallower breathers during normoxia as well as hypoxia. In addition, the maximum hypoxic ventilatory response of the OD mice was lower than that of the WT control group and the peak increase in minute ventilation (.V(max)-.V(normoxia)) was greater in WT control than the OD mice (P=0.02). Since the lung development and NEB morphology in OD mice were comparable to the WT control mice, the observed differences implicate NADPH oxidase as an O(2) sensor involved in neonatal ventilatory control, possibly modulated via pulmonary NEBs. |
