Continuous inhalation of carbon monoxide attenuates hypoxic pulmonary hypertension development presumably through activation of BKCa channels
We tested the hypothesis that inhalation of a low concentration of exogenous carbon monoxide (CO) attenuates the development of hypoxic pulmonary artery hypertension by activation of large-conductance voltage and Ca(2+)-activated K(+) channels (BK(Ca)). The BK(Ca) activity was measured using whole-c...
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| Veröffentlicht in: | Cardiovascular research 2005-02, Vol.65 (3), p.751-761 |
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| creator | DUBUIS, Eric POTIER, Marie RUI WANG VANDIER, Christophe |
| description | We tested the hypothesis that inhalation of a low concentration of exogenous carbon monoxide (CO) attenuates the development of hypoxic pulmonary artery hypertension by activation of large-conductance voltage and Ca(2+)-activated K(+) channels (BK(Ca)).
The BK(Ca) activity was measured using whole-cell and inside-out patch clamp recordings in Wistar rat pulmonary artery (PA) myocytes. Pulmonary artery pressures were measured in vivo and membrane potentials were recorded in vitro in pressurized resistance arteries.
Chronic CO inhalation slightly increases single-channel conductance of BK(Ca) channels and induces a large increase in the sensitivity of BK(Ca) channels to Ca(2+) of PA myocytes from normoxic and chronic hypoxic rats. Consequently, BK(Ca) currents are increased and play a more prominent role in controlling resting membrane potential of PA myocytes. Chronic CO inhalation also reduces hemodynamic changes induced by chronic hypoxia and attenuates hypoxic pulmonary artery hypertension.
Chronic inhalation of CO attenuates hypoxic pulmonary artery hypertension development presumably through activation of BK(Ca) channels. These results highlight the potential use of CO as a novel avenue for research on the treatment of pulmonary artery hypertension (PAHT) in a similar manner to another gasotransmitter, nitric oxide. |
| doi_str_mv | 10.1016/j.cardiores.2004.11.007 |
| format | Article |
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The BK(Ca) activity was measured using whole-cell and inside-out patch clamp recordings in Wistar rat pulmonary artery (PA) myocytes. Pulmonary artery pressures were measured in vivo and membrane potentials were recorded in vitro in pressurized resistance arteries.
Chronic CO inhalation slightly increases single-channel conductance of BK(Ca) channels and induces a large increase in the sensitivity of BK(Ca) channels to Ca(2+) of PA myocytes from normoxic and chronic hypoxic rats. Consequently, BK(Ca) currents are increased and play a more prominent role in controlling resting membrane potential of PA myocytes. Chronic CO inhalation also reduces hemodynamic changes induced by chronic hypoxia and attenuates hypoxic pulmonary artery hypertension.
Chronic inhalation of CO attenuates hypoxic pulmonary artery hypertension development presumably through activation of BK(Ca) channels. These results highlight the potential use of CO as a novel avenue for research on the treatment of pulmonary artery hypertension (PAHT) in a similar manner to another gasotransmitter, nitric oxide.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/j.cardiores.2004.11.007</identifier><identifier>PMID: 15664403</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Biological and medical sciences ; Calcium - pharmacology ; Carbon Monoxide - administration & dosage ; Carbon Monoxide - therapeutic use ; Cardiology. Vascular system ; Cell Polarity - drug effects ; Chronic Disease ; Drug Administration Schedule ; Hemodynamics - drug effects ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - physiopathology ; Hypertension, Pulmonary - prevention & control ; Hypoxia - complications ; Hypoxia - physiopathology ; Male ; Medical sciences ; Membrane Potentials - drug effects ; Muscle Cells - drug effects ; Muscle Cells - physiology ; Muscle, Smooth - drug effects ; Muscle, Smooth - physiopathology ; Patch-Clamp Techniques ; Peptides - pharmacology ; Pneumology ; Potassium Channels, Calcium-Activated - drug effects ; Potassium Channels, Calcium-Activated - physiology ; Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases ; Rats ; Rats, Wistar</subject><ispartof>Cardiovascular research, 2005-02, Vol.65 (3), p.751-761</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16437648$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15664403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DUBUIS, Eric</creatorcontrib><creatorcontrib>POTIER, Marie</creatorcontrib><creatorcontrib>RUI WANG</creatorcontrib><creatorcontrib>VANDIER, Christophe</creatorcontrib><title>Continuous inhalation of carbon monoxide attenuates hypoxic pulmonary hypertension development presumably through activation of BKCa channels</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>We tested the hypothesis that inhalation of a low concentration of exogenous carbon monoxide (CO) attenuates the development of hypoxic pulmonary artery hypertension by activation of large-conductance voltage and Ca(2+)-activated K(+) channels (BK(Ca)).
The BK(Ca) activity was measured using whole-cell and inside-out patch clamp recordings in Wistar rat pulmonary artery (PA) myocytes. Pulmonary artery pressures were measured in vivo and membrane potentials were recorded in vitro in pressurized resistance arteries.
Chronic CO inhalation slightly increases single-channel conductance of BK(Ca) channels and induces a large increase in the sensitivity of BK(Ca) channels to Ca(2+) of PA myocytes from normoxic and chronic hypoxic rats. Consequently, BK(Ca) currents are increased and play a more prominent role in controlling resting membrane potential of PA myocytes. Chronic CO inhalation also reduces hemodynamic changes induced by chronic hypoxia and attenuates hypoxic pulmonary artery hypertension.
Chronic inhalation of CO attenuates hypoxic pulmonary artery hypertension development presumably through activation of BK(Ca) channels. These results highlight the potential use of CO as a novel avenue for research on the treatment of pulmonary artery hypertension (PAHT) in a similar manner to another gasotransmitter, nitric oxide.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Carbon Monoxide - administration & dosage</subject><subject>Carbon Monoxide - therapeutic use</subject><subject>Cardiology. Vascular system</subject><subject>Cell Polarity - drug effects</subject><subject>Chronic Disease</subject><subject>Drug Administration Schedule</subject><subject>Hemodynamics - drug effects</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Hypertension, Pulmonary - prevention & control</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Muscle Cells - drug effects</subject><subject>Muscle Cells - physiology</subject><subject>Muscle, Smooth - drug effects</subject><subject>Muscle, Smooth - physiopathology</subject><subject>Patch-Clamp Techniques</subject><subject>Peptides - pharmacology</subject><subject>Pneumology</subject><subject>Potassium Channels, Calcium-Activated - drug effects</subject><subject>Potassium Channels, Calcium-Activated - physiology</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Rats</subject><subject>Rats, Wistar</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtu1DAUhi0EokPhFcAb2CW149tkCSNuaiU2ZT06sU-IK8cOsVMxD9F3xhUDrM7l_86VkDectZxxfXXXWlidTyvmtmNMtpy3jJknZMeNUo3opHpKdoyxfaOFFhfkRc53NVTKyOfkgiutpWRiRx4OKRYft7Rl6uMEAYpPkaaR1gFD9eYU0y_vkEIpGDcomOl0WmrO0mULVYb19JjBter5sdjhPYa0zBgLXeqG2wxDONEyrWn7MVGwxd__G_Ph-gDUThAjhvySPBshZHx1tpfk-6ePt4cvzc23z18P72-apRN9acZe9XxwuhdDJ6DXwFknNIhODQ71yAzj_R6Nc6M1uK_qiJYbByCVRDH04pK8-9N3WdPPDXM5zj5bDAEi1k8ctRGm6zSv4OszuA0zuuOy-rnee_z7wAq8PQOQLYRxhWh9_s9pKYyWe_Eb1LeHnA</recordid><startdate>20050215</startdate><enddate>20050215</enddate><creator>DUBUIS, Eric</creator><creator>POTIER, Marie</creator><creator>RUI WANG</creator><creator>VANDIER, Christophe</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20050215</creationdate><title>Continuous inhalation of carbon monoxide attenuates hypoxic pulmonary hypertension development presumably through activation of BKCa channels</title><author>DUBUIS, Eric ; POTIER, Marie ; RUI WANG ; VANDIER, Christophe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p239t-f9591bd693b23a96a10236a325bde6f070198e7ddfc7e8a10fec17daa454e3b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Carbon Monoxide - administration & dosage</topic><topic>Carbon Monoxide - therapeutic use</topic><topic>Cardiology. Vascular system</topic><topic>Cell Polarity - drug effects</topic><topic>Chronic Disease</topic><topic>Drug Administration Schedule</topic><topic>Hemodynamics - drug effects</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Hypertension, Pulmonary - prevention & control</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Muscle Cells - drug effects</topic><topic>Muscle Cells - physiology</topic><topic>Muscle, Smooth - drug effects</topic><topic>Muscle, Smooth - physiopathology</topic><topic>Patch-Clamp Techniques</topic><topic>Peptides - pharmacology</topic><topic>Pneumology</topic><topic>Potassium Channels, Calcium-Activated - drug effects</topic><topic>Potassium Channels, Calcium-Activated - physiology</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</topic><topic>Rats</topic><topic>Rats, Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DUBUIS, Eric</creatorcontrib><creatorcontrib>POTIER, Marie</creatorcontrib><creatorcontrib>RUI WANG</creatorcontrib><creatorcontrib>VANDIER, Christophe</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DUBUIS, Eric</au><au>POTIER, Marie</au><au>RUI WANG</au><au>VANDIER, Christophe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Continuous inhalation of carbon monoxide attenuates hypoxic pulmonary hypertension development presumably through activation of BKCa channels</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2005-02-15</date><risdate>2005</risdate><volume>65</volume><issue>3</issue><spage>751</spage><epage>761</epage><pages>751-761</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>We tested the hypothesis that inhalation of a low concentration of exogenous carbon monoxide (CO) attenuates the development of hypoxic pulmonary artery hypertension by activation of large-conductance voltage and Ca(2+)-activated K(+) channels (BK(Ca)).
The BK(Ca) activity was measured using whole-cell and inside-out patch clamp recordings in Wistar rat pulmonary artery (PA) myocytes. Pulmonary artery pressures were measured in vivo and membrane potentials were recorded in vitro in pressurized resistance arteries.
Chronic CO inhalation slightly increases single-channel conductance of BK(Ca) channels and induces a large increase in the sensitivity of BK(Ca) channels to Ca(2+) of PA myocytes from normoxic and chronic hypoxic rats. Consequently, BK(Ca) currents are increased and play a more prominent role in controlling resting membrane potential of PA myocytes. Chronic CO inhalation also reduces hemodynamic changes induced by chronic hypoxia and attenuates hypoxic pulmonary artery hypertension.
Chronic inhalation of CO attenuates hypoxic pulmonary artery hypertension development presumably through activation of BK(Ca) channels. These results highlight the potential use of CO as a novel avenue for research on the treatment of pulmonary artery hypertension (PAHT) in a similar manner to another gasotransmitter, nitric oxide.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>15664403</pmid><doi>10.1016/j.cardiores.2004.11.007</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Calcium - pharmacology Carbon Monoxide - administration & dosage Carbon Monoxide - therapeutic use Cardiology. Vascular system Cell Polarity - drug effects Chronic Disease Drug Administration Schedule Hemodynamics - drug effects Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology Hypertension, Pulmonary - prevention & control Hypoxia - complications Hypoxia - physiopathology Male Medical sciences Membrane Potentials - drug effects Muscle Cells - drug effects Muscle Cells - physiology Muscle, Smooth - drug effects Muscle, Smooth - physiopathology Patch-Clamp Techniques Peptides - pharmacology Pneumology Potassium Channels, Calcium-Activated - drug effects Potassium Channels, Calcium-Activated - physiology Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Rats Rats, Wistar |
| title | Continuous inhalation of carbon monoxide attenuates hypoxic pulmonary hypertension development presumably through activation of BKCa channels |
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