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Endothelium-dependent vasodilators do not cause propagated intercellular Ca2+ waves in vascular endothelial
H M Honda1, J I Goldhaber, L L Demer
1Department of Medicine, University of California, Los Angeles 90095-1679, USA.
Cell Calcium
|February 1, 1996
Summary
Upstream vasodilation is not caused by calcium ion waves spreading between endothelial cells. This study found that common vasodilators do not trigger this intercellular calcium signaling, suggesting alternative mechanisms are at play.
Area of Science:
- Cardiovascular Physiology
- Endothelial Cell Biology
- Vascular Signaling
Background:
- Local application of vasoactive agents influences vasomotor tone both downstream and upstream.
- The precise mechanisms driving upstream signal propagation remain largely unknown.
- Intercellular propagation of endothelial cell (EC) intracellular calcium ([Ca2+]i) increases occurs following mechanical stimulation.
Purpose of the Study:
- To investigate whether increases in EC [Ca2+]i induced by local application of endothelium-dependent vasodilators can spread intercellularly.
- To determine if EC [Ca2+]i waves mediate upstream vasodilation.
Main Methods:
- Utilized endothelial cell monolayers.
- Applied endothelium-dependent vasodilators (ATP, bradykinin, acetylcholine) locally.
- Monitored and analyzed intercellular propagation of EC [Ca2+]i levels.
Main Results:
- Localized application of ATP, bradykinin, and acetylcholine did not induce significant propagation of EC [Ca2+]i increases across the monolayer.
- The response differed markedly from that observed with mechanical stimulation.
Conclusions:
- Upstream vasodilation in response to endothelium-dependent vasodilators is not mediated by the propagation of EC [Ca2+]i waves.
- Alternative electrical or chemical signaling pathways are likely responsible for upstream vasodilation.