Murrant C L, Duza T, Kim M B, Cohen K D, Sarelius I H
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Acta Physiol Scand. 2004 Mar;180(3):231-8. doi: 10.1046/j.0001-6772.2003.01241.x.
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.
We tested the hypothesis that changes in endothelial cell calcium (Ca2+) are involved in this dilation.
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.
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.
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.
