Abstract
Pannexin 1 (Panx1) is involved in endothelium-dependent vasodilation in large arteries, but the exact mechanistic role remains poorly understood. We hypothesized that Panx1 facilitates large vessel relaxations regulating endothelium-derived hyperpolarization (EDH)-like mechanisms. The EDH-like component of acetylcholine-induced relaxation of saphenous arteries studied in isometric myograph after inhibition of NO-synthase and cyclooxygenase was significantly impaired in mice with genetically ablated Panx1 (KO) relative to that in the wild type (WT) mice. Application of P1-receptor antagonist and apyrase significantly reduced this component in WT, but not in KO mice, indicating participation of ATP released via Panx1 in the EDH-like relaxation.
Original language | English (US) |
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Pages (from-to) | 1164-1170 |
Number of pages | 7 |
Journal | FEBS letters |
Volume | 589 |
Issue number | 10 |
DOIs | |
State | Published - Apr 28 2015 |
Keywords
- ATP
- EDHF
- Endothelium
- Endothelium-derived hyperpolarization
- Knockout mice
- Pannexin 1
- Pannexins
- Saphenous artery
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology