Ground reaction forces during locomotion in simulated microgravity

The role of ET and KATP channel in hypoxia-induced negative chronotropic effect of pacemaker cells in rabbit sinoatrial node was studied with intracellular microelectrode technique. The results obtained were as follows: (1) Hypoxia produced a progressive decrease in the velocity of diastolic depolarization (VDD) of pacemaker cells resulting in a reduced rate of pacemaker firing (RPF), and induced a decrease in APD, especially APD50. (2) KATP channel opener cromakalim markedly induced a negative chronotropic effect in a concentration-dependent manner and significantly shortened APD50. KATP channel blocker glibenclamide alleviated the effects of hypoxia on pacemaker cells, thereby suggesting the involvement of KATP channel in the hypoxia-induced effects. (3) By superfusion of ET-1, the hypoxia-induced decrease in RPF was remarkably potentiated and the occurrence of pacemaker arrest was shifted to an earlier time. The hypoxia-induced effects could be effectively attenuated after pretreatment with BQ-123, implying the role of endogenous ET-1 release in hypoxia-induced effects. It is concluded that the negative chronotropic effect and the decrease in APD induced by hypoxia may be attributed to the activation of KATP channel and the release of endogenous ET.