H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway

Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Suarez, Sebastian, Bikiel, Damian Ezequiel, Martí, Marcelo Adrián, Doctorovich, Fabio Ariel
Publicado:	2014
Materias:	calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug nitrogen oxide transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20411723_v5_n_p_Eberhardt http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_20411723_v5_n_p_Eberhardt
record_format	dspace
spelling	paper:paper_20411723_v5_n_p_Eberhardt2023-06-08T16:33:06Z H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway Suarez, Sebastian Bikiel, Damian Ezequiel Martí, Marcelo Adrián Doctorovich, Fabio Ariel calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism. Here we propose that HNO is generated as a result of the reaction of the two gasotransmitters NO and H 2 S. We show that H 2 S and NO production colocalizes with transient receptor potential channel A1 (TRPA1), and that HNO activates the sensory chemoreceptor channel TRPA1 via formation of amino-terminal disulphide bonds, which results in sustained calcium influx. As a consequence, CGRP is released, which induces local and systemic vasodilation. H 2 S-evoked vasodilatatory effects largely depend on NO production and activation of HNO-TRPA1-CGRP pathway. We propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system. © 2014 Macmillan Publishers Limited. All rights reserved. Fil:Suárez, S.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Bikiel, D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Martí, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Doctorovich, F. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2014 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20411723_v5_n_p_Eberhardt http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion
spellingShingle	calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion Suarez, Sebastian Bikiel, Damian Ezequiel Martí, Marcelo Adrián Doctorovich, Fabio Ariel H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
topic_facet	calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion
description	Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism. Here we propose that HNO is generated as a result of the reaction of the two gasotransmitters NO and H 2 S. We show that H 2 S and NO production colocalizes with transient receptor potential channel A1 (TRPA1), and that HNO activates the sensory chemoreceptor channel TRPA1 via formation of amino-terminal disulphide bonds, which results in sustained calcium influx. As a consequence, CGRP is released, which induces local and systemic vasodilation. H 2 S-evoked vasodilatatory effects largely depend on NO production and activation of HNO-TRPA1-CGRP pathway. We propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system. © 2014 Macmillan Publishers Limited. All rights reserved.
author	Suarez, Sebastian Bikiel, Damian Ezequiel Martí, Marcelo Adrián Doctorovich, Fabio Ariel
author_facet	Suarez, Sebastian Bikiel, Damian Ezequiel Martí, Marcelo Adrián Doctorovich, Fabio Ariel
author_sort	Suarez, Sebastian
title	H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
title_short	H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
title_full	H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
title_fullStr	H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
title_full_unstemmed	H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
title_sort	h2s and no cooperatively regulate vascular tone by activating a neuroendocrine hno-trpa1-cgrp signalling pathway
publishDate	2014
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_20411723_v5_n_p_Eberhardt http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt
work_keys_str_mv	AT suarezsebastian h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT bikieldamianezequiel h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT martimarceloadrian h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT doctorovichfabioariel h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway
_version_	1768542524532588544

H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway

Ejemplares similares