There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
Communication of agonist-induced membrane potential changes along blood vessels has
been proposed to contribute to the coordination of microvascular function. Factors
mediating septic shock may compromise this coordination. Using electrophysiology in
a simplified in vitro model of endothelial cells grown as capillary-like structures,
we aimed to determine (i) the effect of lipopolysaccharide (LPS) on endothelial cell
membrane potential responses to ATP and KCl and (ii) the effect of LPS and nitric
oxide (NO) on cell-to-cell communication. Treatment of ‘capillaries’ with LPS (10
µg/ml for 1 h) did not affect local responsiveness to ATP or KCl, but reduced cell
communication by a tyrosine-kinase-dependent mechanism. Treatment of ‘capillaries’
with the NO donor DETA (100 µ M ) or the NO synthase inhibitor L-NAME (100 µ M ) had
no effect on cell communication or the response to LPS. Endogenous NO production,
stimulated by LPS + interferon-γ (100 U/ml) treatment, also had no effect on cell
communication beyond that of LPS alone. We conclude that LPS, but not NO, can modulate
conduction of agonist-induced electrical responses along endothelial capillary-like
structures in vitro.