Key result
Nitric oxide dose-dependently decreased ET-1-stimulated Ca2+ mobilization and induced F-actin filament rearrangement in human brain microvascular endothelial cells.
Hypothesis-generating for nitric oxide in cerebral endothelial signaling; leaves open in vivo or clinical translation.
A functional interrelation between nitric oxide (NO), the endothelial-derived vasodilating factor, and endothelin 1 (ET-1), the potent vasoconstrictive peptide, was investigated in microvascular endothelium of human brain. Nor-1 dose-dependently decreased the ET-1-stimulated mobilization of Ca2+. This response was mimicked with cGMP and abrogated by inhibitors of guanylyl cyclase or cGMP-dependent protein kinase G. These findings indicate that NO and ET-1 interactions involved in modulation of intracellular Ca2+ are mediated by cGMP/protein kinase G. In addition, Nor-1-mediated effects were associated with rearrangements of cytoskeleton F-actin filaments. The results suggest mechanisms by which NO-ET-1 interactions may contribute to regulation of microvascular function.
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McCarron et al. (1999) studied this question. Nor-1 (Nitric Oxide donor) was evaluated on ET-1-stimulated mobilization of Ca2+. Nitric oxide dose-dependently decreased ET-1-stimulated Ca2+ mobilization and induced F-actin filament rearrangement in human brain microvascular endothelial cells.
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