期刊
EXPERIMENTAL PHYSIOLOGY
卷 99, 期 11, 页码 1453-1466出版社
WILEY
DOI: 10.1113/expphysiol.2014.080069
关键词
-
类别
资金
- British Heart Foundation [RG/12/6/29670]
- Japan Society for the Promotion of Science [24790206]
- National Institutes of Health [R01 NS069220]
- Royal Society
- Daiwa Anglo-Japanese Foundation
- Takeda Science Foundation
- Ichiro Kanehara Foundation
- British Heart Foundation [PG/11/47/28980, RG/12/6/29670] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [24790206] Funding Source: KAKEN
Brainstem hypoperfusion is a major excitant of sympathetic activity triggering hypertension, but the exact mechanisms involved remain incompletely understood. A major source of excitatory drive to preganglionic sympathetic neurons originates from the ongoing activity of premotor neurons in the rostral ventrolateral medulla (RVLM sympathetic premotor neurons). The chemosensitivity profile of physiologically characterized RVLM sympathetic premotor neurons during hypoxia and hypercapnia remains unclear. We examined whether physiologically characterized RVLM sympathetic premotor neurons can sense brainstem ischaemia intrinsically. We addressed this issue in a unique in situ arterially perfused preparation before and after a complete blockade of fast excitatory and inhibitory synaptic transmission. During hypercapnic hypoxia, respiratory modulation of RVLM sympathetic premotor neurons was lost, but tonic firing of most RVLM sympathetic premotor neurons was elevated. After blockade of fast excitatory and inhibitory synaptic transmission, RVLM sympathetic premotor neurons continued to fire and exhibited an excitatory firing response to hypoxia but not hypercapnia. This study suggests that RVLM sympathetic premotor neurons can sustain high levels of neuronal discharge when oxygen is scarce. The intrinsic ability of RVLM sympathetic premotor neurons to maintain responsivity to brainstem hypoxia is an important mechanism ensuring adequate arterial pressure, essential for maintaining cerebral perfusion in the face of depressed ventilation and/or high cerebral vascular resistance.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据