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Published on: September 22, 2011
Arteriolar dilations induced by contraction of hamster cremaster muscle are dependent on changes in endothelial cell
1Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Insights
Muscle contraction triggers arteriolar dilation, requiring an initial transient change in endothelial cell calcium (Ca2+). However, sustained dilation occurs independently of global Ca2+ levels.
Area of Science:
- Physiology
- Vascular Biology
- Cell Signaling
Background:
- Muscle contraction causes arteriolar dilation in nearby regions.
- The specific cells and signaling pathways responsible for this dilation are not fully understood.
Purpose of the Study:
- To investigate the role of endothelial cell calcium (Ca2+) in muscle contraction-induced arteriolar dilation.
Main Methods:
- Stimulated muscle fibers adjacent to arterioles and measured arteriolar diameter.
- Used BAPTA to chelate endothelial cell Ca2+ and Fura-PE3 to monitor Ca2+ levels during muscle contraction.
Main Results:
- Chelating endothelial cell Ca2+ abolished muscle contraction-induced dilation.
- While initial dilation required Ca2+, sustained dilation occurred without detectable global Ca2+ changes in endothelial cells.
Conclusions:
- Endothelial cell Ca2+ transients are crucial for initiating muscle contraction-induced arteriolar dilation.
- Mechanisms independent of global endothelial cell Ca2+ maintain dilation after contraction ceases.
Unlabelled:
Muscle contraction initiates microvascular arteriolar dilation in regions directly overlapping the active fibres but the cells (vascular smooth muscle cells, endothelial cells) responsible for producing the dilation and the underlying signalling mechanisms are unknown.
Aims:
We tested the hypothesis that changes in endothelial cell calcium (Ca2+) are involved in this dilation.
Methods:
Four to five muscle fibres lying approximately perpendicular to arterioles (maximum diameter approximately 40 microm) were stimulated (4 Hz, 4-20 V, 0.4 ms duration) and observations were made at the site of muscle fibre/arteriole overlap.
Results:
Chelation of endothelial cell Ca2+ (with BAPTA) abolished dilations to 120 s of muscle contraction (5.6 +/- 1.5 microm in controls vs. 0.51 +/- 1.2 microm with BAPTA, n = 6), indicating that changes in endothelial cell Ca2+ are required for the response. To determine the time frame of the Ca2+ signal, we monitored whole endothelial cell Ca2+ (with Fura-PE3) prior to and following either 120 (n = 13), 30 (n = 9) or 10 (n = 9) s of muscle contraction. In all instances, no changes in Ca2+ were observed despite typical dilator responses.
Conclusions:
These data indicate that (i) the initiation of muscle contraction-induced arteriolar dilations depends on a change in endothelial cell Ca2+, which must be a transient event that takes place early/during stimulation, and (ii) maintenance of the dilation after contraction occurs via mechanisms that are independent of changes in global Ca2+ within the cell.
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