Role of rat vascular KATP channels in setting microvascular oxygen pressure at the onset of contractions

作者

Clark Holdsworth¹ , Scott Ferguson¹ , Jennifer Wright¹ , Alexander Fees¹ , Timothy Musch¹ , David Poole¹

1. Kansas State University

会议/活动

Experimental Biology, April 2014 (San Diego, CA, United States)

海报摘要

Vascular hyperpolarization mediated, in part, by the ATP-sensitive K+ (KATP) channel contributes to exercise-induced increases in skeletal muscle O2 delivery. We hypothesized that KATP channel inhibition via glibenclamide (GLI) would speed the fall of microvascular O2 driving pressure (PO2mv; set by the O2 delivery-O2 utilization ratio), following the onset of muscle contractions. Spinotrapezius PO2mv (phosphorescence quenching) was measured in 12 adult Sprague Dawley rats during 180 s of 1-Hz twitch contractions (~7 V) under control and GLI (5 mg/kg) conditions. Following the onset of contractions the total mean response time was greater with GLI (control: 42.0 ± 14.2, GLI: 79.5 ± 14.7 s). A clear undershoot of the contracting steady-state PO2mv was evident with GLI (15.6 ± 5.3 %) but not control (2.3 ± 1.6 %). This indicates that KATP channel inhibition does not speed PO2mv kinetics during small muscle mass electrical stimulation, but causes a transient mismatch of O2 delivery-O2 utilization prior to stabilizing at the contracting steady-state.

关键词

microcirculation, oxygen diffusion, vascular control, metabolic coupling

研究领域

Anatomy and Physiology

参考文献

暂无数据

基金

暂无数据

补充材料

暂无数据

附加信息

利益冲突

No competing interests were disclosed.

数据可用性声明

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

知识共享许可协议

Copyright © 2022 Holdsworth et al. This is an open access work distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.