Abstract
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.
Original language | English (US) |
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Pages (from-to) | 133-138 |
Number of pages | 6 |
Journal | Journal of Cerebral Blood Flow and Metabolism |
Volume | 19 |
Issue number | 2 |
DOIs | |
State | Published - 1999 |
Keywords
- Actin
- Brain endothelial cells
- Ca Mobilization
- Nitric oxide
- cGMP Endothelin
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Cardiology and Cardiovascular Medicine