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FEBS Lett. 2015 Apr 28;589(10):1164-70. doi: 10.1016/j.febslet.2015.03.018. Epub 2015 Mar 24.

Pannexin 1 facilitates arterial relaxation via an endothelium-derived hyperpolarization mechanism.

Author information

1
State Research Center of the Russian Federation - Institute for Biomedical Problems RAS, Khoroshevskoe shosse 76A, 123007 Moscow, Russia; Faculty of Biology, M.V. Lomonosov Moscow State University, Leninskie Gory 1-12, 119234 Moscow, Russia; Department of Physiology, Russian National Research Medical University, Ostrovityanova Str. 1, 117997 Moscow, Russia. Electronic address: dina.gaynullina@gmail.com.
2
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miller School of Medicine, Miami, FL, United States; Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia.
3
Institute for Information Transmission Problems, Russian Academy of Sciences, Bolshoi Karetny Pereulok 19-1, 127994 Moscow, Russia; Department of Mathematical Methods in Biology, Belozersky Institute, M.V. Lomonosov Moscow State University, Leninskie Gory 1-40, 119991 Moscow, Russia.
4
State Research Center of the Russian Federation - Institute for Biomedical Problems RAS, Khoroshevskoe shosse 76A, 123007 Moscow, Russia; Faculty of Biology, M.V. Lomonosov Moscow State University, Leninskie Gory 1-12, 119234 Moscow, Russia.

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.

KEYWORDS:

ATP; EDHF; Endothelium; Endothelium-derived hyperpolarization; Knockout mice; Pannexin 1; Pannexins; Saphenous artery

PMID:
25819435
DOI:
10.1016/j.febslet.2015.03.018
[Indexed for MEDLINE]
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