抄録
Acute hypoxia elicits a biphasic ventilatory response, initial augmentation and subsequent depression. Although oxygen-sensitive channels of type I cells in the carotid body are considered to be involved in the initial augmentation, the underlying cellular mechanism for the subsequent depression, hypoxic ventilatory decline (HVD), has not been fully elucidated. The purpose of the present study is to examine the role of an ATP-sensitive potassium channel, Kir6.2, in the hypoxic ventilatory response including HVD in the mouse. We serially measured minute ventilation volume (Ve) of the Kir6.2-knockout mouse (Kir6.2-/-: n = 5) exposed to hypoxia (12% O2 in N2: 10min) in an unanesthetized unrestrained state by whole body plethysmography in the 2nd and 4th postnatal weeks. Percent changes from the baseline Ve in the room air were calculated and compared with that in the C57BL/6 mouse (n = 10). In the 2nd postnatal week, there was no difference in the hypoxic ventilatory response between the C57BL/6 and Kir6.2-/- mice. Meanwhile, in the 4th week, the initial augmentation lasted longer, and HVD was much weaker in the Kir6.2-/- than in the C57BL/6. It is concluded that Kir6.2 is involved in the hypoxic ventilatory response including HVD in an age-dependent manner in the mouse. [J Physiol Sci. 2006;56 Suppl:S74]
