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Critical contribution of Na + -Ca 2+ exchanger to the Ca 2+ -mediated vasodilation activated in endothelial cells of resistance arteries
Na -Ca exchanger (NCX) contributes to control the intracellular free Ca concentration ([Ca ] ), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca uptake in the endothelium-dependent vasodilation of rat...
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Published in: | The FASEB journal 2018-04, Vol.32 (4), p.2137-2147 |
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creator | Lillo, Mauricio A Gaete, Pablo S Puebla, Mariela Ardiles, Nicolás M Poblete, Inés Becerra, Alvaro Simon, Felipe Figueroa, Xavier F |
description | Na
-Ca
exchanger (NCX) contributes to control the intracellular free Ca
concentration ([Ca
]
), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca
uptake in the endothelium-dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine-contracted mesenteries, the acetylcholine (ACh)-induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB-R7943, or SN-6. Consistent with that, the ACh-induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB-R7943 and SEA0400, respectively. In addition, both blockers abolished the NO production activated by ACh in intact mesenteric arteries. In contrast, the inhibition of NCXrm did not affect the vasodilator responses induced by the Ca
ionophore, ionomycin, and the NO donor, S-nitroso- N-acetylpenicillamine. Furthermore, SEA0400, KB-R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca
]
induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO-synthesizing enzyme, eNOS, and NCX1 were associated in endothelial cell caveolae of intact mesenteric resistance arteries. These results indicate that the activation of NCXrm has a central role in Ca
-mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.-Lillo, M. A., Gaete, P. S., Puebla, M., Ardiles, N. M., Poblete, I., Becerra, A., Simon, F., Figueroa, X. F. Critical contribution of Na
-Ca
exchanger to the Ca
-mediated vasodilation activated in endothelial cells of resistance arteries. |
doi_str_mv | 10.1096/fj.201700365RR |
format | article |
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-Ca
exchanger (NCX) contributes to control the intracellular free Ca
concentration ([Ca
]
), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca
uptake in the endothelium-dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine-contracted mesenteries, the acetylcholine (ACh)-induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB-R7943, or SN-6. Consistent with that, the ACh-induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB-R7943 and SEA0400, respectively. In addition, both blockers abolished the NO production activated by ACh in intact mesenteric arteries. In contrast, the inhibition of NCXrm did not affect the vasodilator responses induced by the Ca
ionophore, ionomycin, and the NO donor, S-nitroso- N-acetylpenicillamine. Furthermore, SEA0400, KB-R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca
]
induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO-synthesizing enzyme, eNOS, and NCX1 were associated in endothelial cell caveolae of intact mesenteric resistance arteries. These results indicate that the activation of NCXrm has a central role in Ca
-mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.-Lillo, M. A., Gaete, P. S., Puebla, M., Ardiles, N. M., Poblete, I., Becerra, A., Simon, F., Figueroa, X. F. Critical contribution of Na
-Ca
exchanger to the Ca
-mediated vasodilation activated in endothelial cells of resistance arteries.</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.201700365RR</identifier><identifier>PMID: 29217667</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Calcium - metabolism ; Cells, Cultured ; Endothelial Cells - metabolism ; Endothelium, Vascular - cytology ; Endothelium, Vascular - metabolism ; Male ; Mesenteric Arteries - cytology ; Mesenteric Arteries - metabolism ; Mesenteric Arteries - physiology ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - physiology ; Myocytes, Smooth Muscle - metabolism ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium-Calcium Exchanger - antagonists & inhibitors ; Sodium-Calcium Exchanger - metabolism ; Vasodilation</subject><ispartof>The FASEB journal, 2018-04, Vol.32 (4), p.2137-2147</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c147r-5d646fd24cc85a16dfa6de75816a9cd32565ca4ea0a82f0c2f363ca360f240503</citedby><cites>FETCH-LOGICAL-c147r-5d646fd24cc85a16dfa6de75816a9cd32565ca4ea0a82f0c2f363ca360f240503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29217667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lillo, Mauricio A</creatorcontrib><creatorcontrib>Gaete, Pablo S</creatorcontrib><creatorcontrib>Puebla, Mariela</creatorcontrib><creatorcontrib>Ardiles, Nicolás M</creatorcontrib><creatorcontrib>Poblete, Inés</creatorcontrib><creatorcontrib>Becerra, Alvaro</creatorcontrib><creatorcontrib>Simon, Felipe</creatorcontrib><creatorcontrib>Figueroa, Xavier F</creatorcontrib><title>Critical contribution of Na + -Ca 2+ exchanger to the Ca 2+ -mediated vasodilation activated in endothelial cells of resistance arteries</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>Na
-Ca
exchanger (NCX) contributes to control the intracellular free Ca
concentration ([Ca
]
), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca
uptake in the endothelium-dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine-contracted mesenteries, the acetylcholine (ACh)-induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB-R7943, or SN-6. Consistent with that, the ACh-induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB-R7943 and SEA0400, respectively. In addition, both blockers abolished the NO production activated by ACh in intact mesenteric arteries. In contrast, the inhibition of NCXrm did not affect the vasodilator responses induced by the Ca
ionophore, ionomycin, and the NO donor, S-nitroso- N-acetylpenicillamine. Furthermore, SEA0400, KB-R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca
]
induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO-synthesizing enzyme, eNOS, and NCX1 were associated in endothelial cell caveolae of intact mesenteric resistance arteries. These results indicate that the activation of NCXrm has a central role in Ca
-mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.-Lillo, M. A., Gaete, P. S., Puebla, M., Ardiles, N. M., Poblete, I., Becerra, A., Simon, F., Figueroa, X. F. Critical contribution of Na
-Ca
exchanger to the Ca
-mediated vasodilation activated in endothelial cells of resistance arteries.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Cells, Cultured</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Male</subject><subject>Mesenteric Arteries - cytology</subject><subject>Mesenteric Arteries - metabolism</subject><subject>Mesenteric Arteries - physiology</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sodium-Calcium Exchanger - antagonists & inhibitors</subject><subject>Sodium-Calcium Exchanger - metabolism</subject><subject>Vasodilation</subject><issn>0892-6638</issn><issn>1530-6860</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpNkE1LAzEQhoMotlavHiX3snWS7M5uj1L8AlEoel6m-bAp292SpEX_gT_bfqh4GniZ5x3mYexSwEjAGK_dYiRBlAAKi-n0iPVFoSDDCuGY9aEaywxRVT12FuMCAAQIPGU9OZaiRCz77GsSfPKaGq67NgU_Wyfftbxz_Jn4kGcT4nLI7YeeU_tuA08dT3PLD3G2tMZTsoZvKHbGN7SHSSe_2ce-5bY13ZZo_O6EbZq46w42-pio1ZZTSDZ4G8_ZiaMm2oufOWBvd7evk4fs6eX-cXLzlGmRlyErDObojMy1rgoSaByhsWVRCaSxNkoWWGjKLQFV0oGWTqHSpBCczKEANWCjQ68OXYzBunoV_JLCZy2g3imt3aL-p3QLXB2A1Xq2_fdv_deh-gbc0nKs</recordid><startdate>201804</startdate><enddate>201804</enddate><creator>Lillo, Mauricio A</creator><creator>Gaete, Pablo S</creator><creator>Puebla, Mariela</creator><creator>Ardiles, Nicolás M</creator><creator>Poblete, Inés</creator><creator>Becerra, Alvaro</creator><creator>Simon, Felipe</creator><creator>Figueroa, Xavier F</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201804</creationdate><title>Critical contribution of Na + -Ca 2+ exchanger to the Ca 2+ -mediated vasodilation activated in endothelial cells of resistance arteries</title><author>Lillo, Mauricio A ; Gaete, Pablo S ; Puebla, Mariela ; Ardiles, Nicolás M ; Poblete, Inés ; Becerra, Alvaro ; Simon, Felipe ; Figueroa, Xavier F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c147r-5d646fd24cc85a16dfa6de75816a9cd32565ca4ea0a82f0c2f363ca360f240503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Cells, Cultured</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Male</topic><topic>Mesenteric Arteries - cytology</topic><topic>Mesenteric Arteries - metabolism</topic><topic>Mesenteric Arteries - physiology</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sodium-Calcium Exchanger - antagonists & inhibitors</topic><topic>Sodium-Calcium Exchanger - metabolism</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lillo, Mauricio A</creatorcontrib><creatorcontrib>Gaete, Pablo S</creatorcontrib><creatorcontrib>Puebla, Mariela</creatorcontrib><creatorcontrib>Ardiles, Nicolás M</creatorcontrib><creatorcontrib>Poblete, Inés</creatorcontrib><creatorcontrib>Becerra, Alvaro</creatorcontrib><creatorcontrib>Simon, Felipe</creatorcontrib><creatorcontrib>Figueroa, Xavier F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>The FASEB journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lillo, Mauricio A</au><au>Gaete, Pablo S</au><au>Puebla, Mariela</au><au>Ardiles, Nicolás M</au><au>Poblete, Inés</au><au>Becerra, Alvaro</au><au>Simon, Felipe</au><au>Figueroa, Xavier F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Critical contribution of Na + -Ca 2+ exchanger to the Ca 2+ -mediated vasodilation activated in endothelial cells of resistance arteries</atitle><jtitle>The FASEB journal</jtitle><addtitle>FASEB J</addtitle><date>2018-04</date><risdate>2018</risdate><volume>32</volume><issue>4</issue><spage>2137</spage><epage>2147</epage><pages>2137-2147</pages><issn>0892-6638</issn><eissn>1530-6860</eissn><abstract>Na
-Ca
exchanger (NCX) contributes to control the intracellular free Ca
concentration ([Ca
]
), but the functional activation of NCX reverse mode (NCXrm) in endothelial cells is controversial. We evaluated the participation of NCXrm-mediated Ca
uptake in the endothelium-dependent vasodilation of rat isolated mesenteric arterial beds. In phenylephrine-contracted mesenteries, the acetylcholine (ACh)-induced vasodilation was abolished by treatment with the NCXrm blockers SEA0400, KB-R7943, or SN-6. Consistent with that, the ACh-induced hyperpolarization observed in primary cultures of mesenteric endothelial cells and in smooth muscle of isolated mesenteric resistance arteries was attenuated by KB-R7943 and SEA0400, respectively. In addition, both blockers abolished the NO production activated by ACh in intact mesenteric arteries. In contrast, the inhibition of NCXrm did not affect the vasodilator responses induced by the Ca
ionophore, ionomycin, and the NO donor, S-nitroso- N-acetylpenicillamine. Furthermore, SEA0400, KB-R7943, and a small interference RNA directed against NCX1 blunted the increase in [Ca
]
induced by ACh or ATP in cultured endothelial cells. The analysis by proximity ligation assay showed that the NO-synthesizing enzyme, eNOS, and NCX1 were associated in endothelial cell caveolae of intact mesenteric resistance arteries. These results indicate that the activation of NCXrm has a central role in Ca
-mediated vasodilation initiated by ACh in endothelial cells of resistance arteries.-Lillo, M. A., Gaete, P. S., Puebla, M., Ardiles, N. M., Poblete, I., Becerra, A., Simon, F., Figueroa, X. F. Critical contribution of Na
-Ca
exchanger to the Ca
-mediated vasodilation activated in endothelial cells of resistance arteries.</abstract><cop>United States</cop><pmid>29217667</pmid><doi>10.1096/fj.201700365RR</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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source | Wiley |
subjects | Animals Calcium - metabolism Cells, Cultured Endothelial Cells - metabolism Endothelium, Vascular - cytology Endothelium, Vascular - metabolism Male Mesenteric Arteries - cytology Mesenteric Arteries - metabolism Mesenteric Arteries - physiology Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - physiology Myocytes, Smooth Muscle - metabolism Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Rats Rats, Sprague-Dawley Sodium-Calcium Exchanger - antagonists & inhibitors Sodium-Calcium Exchanger - metabolism Vasodilation |
title | Critical contribution of Na + -Ca 2+ exchanger to the Ca 2+ -mediated vasodilation activated in endothelial cells of resistance arteries |
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