Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism

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 compo...
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Autor*in:	Gaynullina, Dina [verfasserIn] Shestopalov, Valery I Panchin, Yury Tarasova, Olga S

Format:	Artikel
Sprache:	Englisch

Erschienen:	2015

Rechteinformationen:	Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved.

Schlagwörter:	Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism

Übergeordnetes Werk:	Enthalten in: FEBS letters - Amsterdam [u.a.] : Elsevier, 1968, 589(2015), 10, Seite 1164-1170
Übergeordnetes Werk:	volume:589 ; year:2015 ; number:10 ; pages:1164-1170

Links:	Volltext Link aufrufen Link aufrufen

DOI / URN:	10.1016/j.febslet.2015.03.018

Katalog-ID:	OLC1965546048

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520			\|a 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice.
540			\|a Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies
540			\|a Copyright © 2015 Federation of European Biochemical Societies. All rights reserved.
650		4	\|a Saphenous artery
650		4	\|a Endothelium-derived hyperpolarization
650		4	\|a Knockout mice
650		4	\|a Endothelium
650		4	\|a ATP
650		4	\|a Pannexins
650		4	\|a EDHF
650		4	\|a Pannexin 1
650		4	\|a Nerve Tissue Proteins - genetics
650		4	\|a Adenosine Triphosphate - genetics
650		4	\|a Receptors, Purinergic P1 - genetics
650		4	\|a Apyrase - pharmacology
650		4	\|a Vasodilation - drug effects
650		4	\|a Purinergic P1 Receptor Antagonists - pharmacology
650		4	\|a Nitric Oxide Synthase Type III - genetics
650		4	\|a Arteries - metabolism
650		4	\|a Nerve Tissue Proteins - metabolism
650		4	\|a Vasodilation - physiology
650		4	\|a Nitric Oxide Synthase Type III - antagonists & inhibitors
650		4	\|a Connexins - genetics
650		4	\|a Connexins - metabolism
650		4	\|a Receptors, Purinergic P1 - metabolism
650		4	\|a Nitric Oxide Synthase Type III - metabolism
650		4	\|a Endothelium, Vascular - metabolism
650		4	\|a Adenosine Triphosphate - metabolism
700	1		\|a Shestopalov, Valery I \|4 oth
700	1		\|a Panchin, Yury \|4 oth
700	1		\|a Tarasova, Olga S \|4 oth
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856	4	1	\|u http://dx.doi.org/10.1016/j.febslet.2015.03.018 \|3 Volltext
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856	4	2	\|u http://www.ncbi.nlm.nih.gov/pubmed/25819435
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Indexfelder

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publishDate	2015
allfields	10.1016/j.febslet.2015.03.018 doi PQ20160617 (DE-627)OLC1965546048 (DE-599)GBVOLC1965546048 (PRQ)c1945-52f012ff71719975627b5b690bf603b50c611d5893cfa188fe77ee5e1fe3901a0 (KEY)0045922420150000589001001164pannexin1facilitatesarterialrelaxationviaanendothe DE-627 ger DE-627 rakwb eng 570 530 610 DNB Gaynullina, Dina verfasserin aut Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice. Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved. Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism Shestopalov, Valery I oth Panchin, Yury oth Tarasova, Olga S oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 589(2015), 10, Seite 1164-1170 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:589 year:2015 number:10 pages:1164-1170 http://dx.doi.org/10.1016/j.febslet.2015.03.018 Volltext http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305 AR 589 2015 10 1164-1170
spelling	10.1016/j.febslet.2015.03.018 doi PQ20160617 (DE-627)OLC1965546048 (DE-599)GBVOLC1965546048 (PRQ)c1945-52f012ff71719975627b5b690bf603b50c611d5893cfa188fe77ee5e1fe3901a0 (KEY)0045922420150000589001001164pannexin1facilitatesarterialrelaxationviaanendothe DE-627 ger DE-627 rakwb eng 570 530 610 DNB Gaynullina, Dina verfasserin aut Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice. Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved. Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism Shestopalov, Valery I oth Panchin, Yury oth Tarasova, Olga S oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 589(2015), 10, Seite 1164-1170 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:589 year:2015 number:10 pages:1164-1170 http://dx.doi.org/10.1016/j.febslet.2015.03.018 Volltext http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305 AR 589 2015 10 1164-1170
allfields_unstemmed	10.1016/j.febslet.2015.03.018 doi PQ20160617 (DE-627)OLC1965546048 (DE-599)GBVOLC1965546048 (PRQ)c1945-52f012ff71719975627b5b690bf603b50c611d5893cfa188fe77ee5e1fe3901a0 (KEY)0045922420150000589001001164pannexin1facilitatesarterialrelaxationviaanendothe DE-627 ger DE-627 rakwb eng 570 530 610 DNB Gaynullina, Dina verfasserin aut Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice. Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved. Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism Shestopalov, Valery I oth Panchin, Yury oth Tarasova, Olga S oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 589(2015), 10, Seite 1164-1170 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:589 year:2015 number:10 pages:1164-1170 http://dx.doi.org/10.1016/j.febslet.2015.03.018 Volltext http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305 AR 589 2015 10 1164-1170
allfieldsGer	10.1016/j.febslet.2015.03.018 doi PQ20160617 (DE-627)OLC1965546048 (DE-599)GBVOLC1965546048 (PRQ)c1945-52f012ff71719975627b5b690bf603b50c611d5893cfa188fe77ee5e1fe3901a0 (KEY)0045922420150000589001001164pannexin1facilitatesarterialrelaxationviaanendothe DE-627 ger DE-627 rakwb eng 570 530 610 DNB Gaynullina, Dina verfasserin aut Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice. Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved. Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism Shestopalov, Valery I oth Panchin, Yury oth Tarasova, Olga S oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 589(2015), 10, Seite 1164-1170 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:589 year:2015 number:10 pages:1164-1170 http://dx.doi.org/10.1016/j.febslet.2015.03.018 Volltext http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305 AR 589 2015 10 1164-1170
allfieldsSound	10.1016/j.febslet.2015.03.018 doi PQ20160617 (DE-627)OLC1965546048 (DE-599)GBVOLC1965546048 (PRQ)c1945-52f012ff71719975627b5b690bf603b50c611d5893cfa188fe77ee5e1fe3901a0 (KEY)0045922420150000589001001164pannexin1facilitatesarterialrelaxationviaanendothe DE-627 ger DE-627 rakwb eng 570 530 610 DNB Gaynullina, Dina verfasserin aut Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier 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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice. Nutzungsrecht: FEBS Letters 589 (2015) 1873-3468 © 2015 Federation of European Biochemical Societies Copyright © 2015 Federation of European Biochemical Societies. All rights reserved. Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism Shestopalov, Valery I oth Panchin, Yury oth Tarasova, Olga S oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 589(2015), 10, Seite 1164-1170 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:589 year:2015 number:10 pages:1164-1170 http://dx.doi.org/10.1016/j.febslet.2015.03.018 Volltext http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305 AR 589 2015 10 1164-1170
language	English
source	Enthalten in FEBS letters 589(2015), 10, Seite 1164-1170 volume:589 year:2015 number:10 pages:1164-1170
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topic_facet	Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism
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authorswithroles_txt_mv	Gaynullina, Dina @@aut@@ Shestopalov, Valery I @@oth@@ Panchin, Yury @@oth@@ Tarasova, Olga S @@oth@@
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author	Gaynullina, Dina
spellingShingle	Gaynullina, Dina ddc 570 misc Saphenous artery misc Endothelium-derived hyperpolarization misc Knockout mice misc Endothelium misc ATP misc Pannexins misc EDHF misc Pannexin 1 misc Nerve Tissue Proteins - genetics misc Adenosine Triphosphate - genetics misc Receptors, Purinergic P1 - genetics misc Apyrase - pharmacology misc Vasodilation - drug effects misc Purinergic P1 Receptor Antagonists - pharmacology misc Nitric Oxide Synthase Type III - genetics misc Arteries - metabolism misc Nerve Tissue Proteins - metabolism misc Vasodilation - physiology misc Nitric Oxide Synthase Type III - antagonists & inhibitors misc Connexins - genetics misc Connexins - metabolism misc Receptors, Purinergic P1 - metabolism misc Nitric Oxide Synthase Type III - metabolism misc Endothelium, Vascular - metabolism misc Adenosine Triphosphate - metabolism Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
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topic_title	570 530 610 DNB Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism Saphenous artery Endothelium-derived hyperpolarization Knockout mice Endothelium ATP Pannexins EDHF Pannexin 1 Nerve Tissue Proteins - genetics Adenosine Triphosphate - genetics Receptors, Purinergic P1 - genetics Apyrase - pharmacology Vasodilation - drug effects Purinergic P1 Receptor Antagonists - pharmacology Nitric Oxide Synthase Type III - genetics Arteries - metabolism Nerve Tissue Proteins - metabolism Vasodilation - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Connexins - genetics Connexins - metabolism Receptors, Purinergic P1 - metabolism Nitric Oxide Synthase Type III - metabolism Endothelium, Vascular - metabolism Adenosine Triphosphate - metabolism
topic	ddc 570 misc Saphenous artery misc Endothelium-derived hyperpolarization misc Knockout mice misc Endothelium misc ATP misc Pannexins misc EDHF misc Pannexin 1 misc Nerve Tissue Proteins - genetics misc Adenosine Triphosphate - genetics misc Receptors, Purinergic P1 - genetics misc Apyrase - pharmacology misc Vasodilation - drug effects misc Purinergic P1 Receptor Antagonists - pharmacology misc Nitric Oxide Synthase Type III - genetics misc Arteries - metabolism misc Nerve Tissue Proteins - metabolism misc Vasodilation - physiology misc Nitric Oxide Synthase Type III - antagonists & inhibitors misc Connexins - genetics misc Connexins - metabolism misc Receptors, Purinergic P1 - metabolism misc Nitric Oxide Synthase Type III - metabolism misc Endothelium, Vascular - metabolism misc Adenosine Triphosphate - metabolism
topic_unstemmed	ddc 570 misc Saphenous artery misc Endothelium-derived hyperpolarization misc Knockout mice misc Endothelium misc ATP misc Pannexins misc EDHF misc Pannexin 1 misc Nerve Tissue Proteins - genetics misc Adenosine Triphosphate - genetics misc Receptors, Purinergic P1 - genetics misc Apyrase - pharmacology misc Vasodilation - drug effects misc Purinergic P1 Receptor Antagonists - pharmacology misc Nitric Oxide Synthase Type III - genetics misc Arteries - metabolism misc Nerve Tissue Proteins - metabolism misc Vasodilation - physiology misc Nitric Oxide Synthase Type III - antagonists & inhibitors misc Connexins - genetics misc Connexins - metabolism misc Receptors, Purinergic P1 - metabolism misc Nitric Oxide Synthase Type III - metabolism misc Endothelium, Vascular - metabolism misc Adenosine Triphosphate - metabolism
topic_browse	ddc 570 misc Saphenous artery misc Endothelium-derived hyperpolarization misc Knockout mice misc Endothelium misc ATP misc Pannexins misc EDHF misc Pannexin 1 misc Nerve Tissue Proteins - genetics misc Adenosine Triphosphate - genetics misc Receptors, Purinergic P1 - genetics misc Apyrase - pharmacology misc Vasodilation - drug effects misc Purinergic P1 Receptor Antagonists - pharmacology misc Nitric Oxide Synthase Type III - genetics misc Arteries - metabolism misc Nerve Tissue Proteins - metabolism misc Vasodilation - physiology misc Nitric Oxide Synthase Type III - antagonists & inhibitors misc Connexins - genetics misc Connexins - metabolism misc Receptors, Purinergic P1 - metabolism misc Nitric Oxide Synthase Type III - metabolism misc Endothelium, Vascular - metabolism misc Adenosine Triphosphate - metabolism
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title	Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
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title_full	Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
author_sort	Gaynullina, Dina
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author_browse	Gaynullina, Dina
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author-letter	Gaynullina, Dina
doi_str_mv	10.1016/j.febslet.2015.03.018
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title_sort	pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
title_auth	Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice.
abstractGer	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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice.
abstract_unstemmed	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. We studied endothelium‐dependent relaxations in control (WT) and Panx1 −/− (KO) mice. The EDH‐like component of endothelium‐dependent relaxation is impaired in KO mice. Blockade of purinergic signaling reduces EDH‐like component in WT, but not in KO mice.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_70 GBV_ILN_211 GBV_ILN_2219 GBV_ILN_4012 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4305
container_issue	10
title_short	Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism
url	http://dx.doi.org/10.1016/j.febslet.2015.03.018 http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2015.03.018/abstract http://www.ncbi.nlm.nih.gov/pubmed/25819435
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author2	Shestopalov, Valery I Panchin, Yury Tarasova, Olga S
author2Str	Shestopalov, Valery I Panchin, Yury Tarasova, Olga S
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doi_str	10.1016/j.febslet.2015.03.018
up_date	2024-07-03T18:13:18.317Z
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Pannexin 1 facilitates arterial relaxation via an endothelium‐derived hyperpolarization mechanism

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