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Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes
Catecholamines (CA) were studied in peripheral human lymphocytes, as well as in the supernatants, after incubation with l-tyrosine and l-dihydroxyphenylalanine ( l-Dopa) for 1 h. The effect that the addition of acetylcholine (ACh), Veratridine, Ionomycin or KCl had on the outflow of norepinephrine (...
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| Published in: | Journal of neuroimmunology 1998-07, Vol.87 (1), p.82-87 |
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| container_title | Journal of neuroimmunology |
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| creator | Musso, Natale R Brenci, Sabrina Indiveri, Francesco Lotti, Gaetano |
| description | Catecholamines (CA) were studied in peripheral human lymphocytes, as well as in the supernatants, after incubation with
l-tyrosine and
l-dihydroxyphenylalanine (
l-Dopa) for 1 h. The effect that the addition of acetylcholine (ACh), Veratridine, Ionomycin or KCl had on the outflow of norepinephrine (NE) from lymphocytes was also studied. The effect of the addition of methoxyverapamil (D600, a Ca
2+ channel blocker) and cholinergic antagonists had on the ACh-induced NE outflow was assessed. CA were determined by HPLC–ECD, both in the supernatant and in the cell lysates.
l-Tyrosine and
l-Dopa significantly (
P |
| doi_str_mv | 10.1016/S0165-5728(98)00057-5 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80017459</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0165572898000575</els_id><sourcerecordid>80017459</sourcerecordid><originalsourceid>FETCH-LOGICAL-c391t-6f881abec9deaaab5ddf1ff75250da7b7074249a686e85231129086920559db03</originalsourceid><addsrcrecordid>eNqFkU1LxDAQhoMouq7-BKEnUbCadJsmOcmy-AULHtRzSJMpjaRNTVql_96uu3jdy-Qwz2SY50XoguBbgklx9zYVmlKW8SvBrzHGlKX0AM0IZ1nK84wcotk_coJOY_zEmNBFLo7RsSgY5jmfIbXU0I9O197ZFlLbmkGDuUm0ctoOTWqgg9ZA2yetD9BNTFeHqSZ-6Cvnf5Iq-CbpINiuhqBcUg-NahM3Nl3t9dhDPENHlXIRznfvHH08PryvntP169PLarlO9UKQPi0qzokqQQsDSqmSGlORqmI0o9goVjLM8iwXquAFcJotCMkE5oXIMKXClHgxR5fbf7vgvwaIvWxs1OCcasEPUfLpepZTsRckRb4RRSeQbkEdfIwBKtkF26gwSoLlJgP5l4HcCJaCy78M5GbuYrdgKBsw_1M76VP_ftuHSce3hSCjttBO3m0A3Uvj7Z4Nv4nemDM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>16400155</pqid></control><display><type>article</type><title>Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes</title><source>ScienceDirect Freedom Collection 2022-2024</source><creator>Musso, Natale R ; Brenci, Sabrina ; Indiveri, Francesco ; Lotti, Gaetano</creator><creatorcontrib>Musso, Natale R ; Brenci, Sabrina ; Indiveri, Francesco ; Lotti, Gaetano</creatorcontrib><description>Catecholamines (CA) were studied in peripheral human lymphocytes, as well as in the supernatants, after incubation with
l-tyrosine and
l-dihydroxyphenylalanine (
l-Dopa) for 1 h. The effect that the addition of acetylcholine (ACh), Veratridine, Ionomycin or KCl had on the outflow of norepinephrine (NE) from lymphocytes was also studied. The effect of the addition of methoxyverapamil (D600, a Ca
2+ channel blocker) and cholinergic antagonists had on the ACh-induced NE outflow was assessed. CA were determined by HPLC–ECD, both in the supernatant and in the cell lysates.
l-Tyrosine and
l-Dopa significantly (
P<0.01) increased intracellular NE. Neither
l-tyrosine,
l-Dopa, nor vehicle induced a detectable outflow of NE to the supernatants. ACh [120
μM], Veratridine [100
μM], Ionomycin [10
μM] and KCl [50 mM] (with or without the simultaneous addition of
l-tyrosine or
l-Dopa) all induced a detectable outflow of NE to the supernatant when added 5 min before the end of incubation. NE was not detectable in the supernatant when the chemicals were added 10 to 20 min before the end of the incubation. When the chemicals were added at lower concentrations, erratic secretion or no secretion whatsoever was observed. D600 [100
μM] was able to significantly (
P<0.01) reduce the ACh-induced NE outflow. Tetraethylammonium (nicotinic antagonist), but not atropine (muscarinic antagonist), significantly (
P<0.001) decreased the ACh-induced NE outflow. The outflow of NE from peripheral human lymphocytes was seen. NE secretion seems to be ACh- and calcium-dependent since Veratridine, Ionomycin and KCl are able to induce Ca
2+ entry by means of various mechanisms. The Ca
2+ channel blocker employed in this study (D600) reduced the ACh-dependent NE outflow. We can conclude that both ACh (through nicotinic receptors) and calcium are involved in the outflow of NE from peripheral human lymphocytes.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/S0165-5728(98)00057-5</identifier><identifier>PMID: 9670848</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Acetylcholine ; Acetylcholine - pharmacology ; Adult ; Calcium ; Calcium - physiology ; Calcium Channel Blockers - pharmacology ; D600 ; Dose-Response Relationship, Drug ; Female ; Gallopamil - pharmacology ; Humans ; Ionomycin ; Ionomycin - pharmacology ; Levodopa - pharmacology ; Lymphocytes ; Lymphocytes - drug effects ; Lymphocytes - metabolism ; Male ; Norepinephrine ; Norepinephrine - metabolism ; Tyrosine - pharmacology ; Veratridine ; Veratridine - pharmacology</subject><ispartof>Journal of neuroimmunology, 1998-07, Vol.87 (1), p.82-87</ispartof><rights>1998 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-6f881abec9deaaab5ddf1ff75250da7b7074249a686e85231129086920559db03</citedby><cites>FETCH-LOGICAL-c391t-6f881abec9deaaab5ddf1ff75250da7b7074249a686e85231129086920559db03</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/9670848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Musso, Natale R</creatorcontrib><creatorcontrib>Brenci, Sabrina</creatorcontrib><creatorcontrib>Indiveri, Francesco</creatorcontrib><creatorcontrib>Lotti, Gaetano</creatorcontrib><title>Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>Catecholamines (CA) were studied in peripheral human lymphocytes, as well as in the supernatants, after incubation with
l-tyrosine and
l-dihydroxyphenylalanine (
l-Dopa) for 1 h. The effect that the addition of acetylcholine (ACh), Veratridine, Ionomycin or KCl had on the outflow of norepinephrine (NE) from lymphocytes was also studied. The effect of the addition of methoxyverapamil (D600, a Ca
2+ channel blocker) and cholinergic antagonists had on the ACh-induced NE outflow was assessed. CA were determined by HPLC–ECD, both in the supernatant and in the cell lysates.
l-Tyrosine and
l-Dopa significantly (
P<0.01) increased intracellular NE. Neither
l-tyrosine,
l-Dopa, nor vehicle induced a detectable outflow of NE to the supernatants. ACh [120
μM], Veratridine [100
μM], Ionomycin [10
μM] and KCl [50 mM] (with or without the simultaneous addition of
l-tyrosine or
l-Dopa) all induced a detectable outflow of NE to the supernatant when added 5 min before the end of incubation. NE was not detectable in the supernatant when the chemicals were added 10 to 20 min before the end of the incubation. When the chemicals were added at lower concentrations, erratic secretion or no secretion whatsoever was observed. D600 [100
μM] was able to significantly (
P<0.01) reduce the ACh-induced NE outflow. Tetraethylammonium (nicotinic antagonist), but not atropine (muscarinic antagonist), significantly (
P<0.001) decreased the ACh-induced NE outflow. The outflow of NE from peripheral human lymphocytes was seen. NE secretion seems to be ACh- and calcium-dependent since Veratridine, Ionomycin and KCl are able to induce Ca
2+ entry by means of various mechanisms. The Ca
2+ channel blocker employed in this study (D600) reduced the ACh-dependent NE outflow. We can conclude that both ACh (through nicotinic receptors) and calcium are involved in the outflow of NE from peripheral human lymphocytes.</description><subject>Acetylcholine</subject><subject>Acetylcholine - pharmacology</subject><subject>Adult</subject><subject>Calcium</subject><subject>Calcium - physiology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>D600</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Gallopamil - pharmacology</subject><subject>Humans</subject><subject>Ionomycin</subject><subject>Ionomycin - pharmacology</subject><subject>Levodopa - pharmacology</subject><subject>Lymphocytes</subject><subject>Lymphocytes - drug effects</subject><subject>Lymphocytes - metabolism</subject><subject>Male</subject><subject>Norepinephrine</subject><subject>Norepinephrine - metabolism</subject><subject>Tyrosine - pharmacology</subject><subject>Veratridine</subject><subject>Veratridine - pharmacology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkU1LxDAQhoMouq7-BKEnUbCadJsmOcmy-AULHtRzSJMpjaRNTVql_96uu3jdy-Qwz2SY50XoguBbgklx9zYVmlKW8SvBrzHGlKX0AM0IZ1nK84wcotk_coJOY_zEmNBFLo7RsSgY5jmfIbXU0I9O197ZFlLbmkGDuUm0ctoOTWqgg9ZA2yetD9BNTFeHqSZ-6Cvnf5Iq-CbpINiuhqBcUg-NahM3Nl3t9dhDPENHlXIRznfvHH08PryvntP169PLarlO9UKQPi0qzokqQQsDSqmSGlORqmI0o9goVjLM8iwXquAFcJotCMkE5oXIMKXClHgxR5fbf7vgvwaIvWxs1OCcasEPUfLpepZTsRckRb4RRSeQbkEdfIwBKtkF26gwSoLlJgP5l4HcCJaCy78M5GbuYrdgKBsw_1M76VP_ftuHSce3hSCjttBO3m0A3Uvj7Z4Nv4nemDM</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>Musso, Natale R</creator><creator>Brenci, Sabrina</creator><creator>Indiveri, Francesco</creator><creator>Lotti, Gaetano</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19980701</creationdate><title>Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes</title><author>Musso, Natale R ; Brenci, Sabrina ; Indiveri, Francesco ; Lotti, Gaetano</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-6f881abec9deaaab5ddf1ff75250da7b7074249a686e85231129086920559db03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acetylcholine</topic><topic>Acetylcholine - pharmacology</topic><topic>Adult</topic><topic>Calcium</topic><topic>Calcium - physiology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>D600</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Gallopamil - pharmacology</topic><topic>Humans</topic><topic>Ionomycin</topic><topic>Ionomycin - pharmacology</topic><topic>Levodopa - pharmacology</topic><topic>Lymphocytes</topic><topic>Lymphocytes - drug effects</topic><topic>Lymphocytes - metabolism</topic><topic>Male</topic><topic>Norepinephrine</topic><topic>Norepinephrine - metabolism</topic><topic>Tyrosine - pharmacology</topic><topic>Veratridine</topic><topic>Veratridine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Musso, Natale R</creatorcontrib><creatorcontrib>Brenci, Sabrina</creatorcontrib><creatorcontrib>Indiveri, Francesco</creatorcontrib><creatorcontrib>Lotti, Gaetano</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Musso, Natale R</au><au>Brenci, Sabrina</au><au>Indiveri, Francesco</au><au>Lotti, Gaetano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>87</volume><issue>1</issue><spage>82</spage><epage>87</epage><pages>82-87</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Catecholamines (CA) were studied in peripheral human lymphocytes, as well as in the supernatants, after incubation with
l-tyrosine and
l-dihydroxyphenylalanine (
l-Dopa) for 1 h. The effect that the addition of acetylcholine (ACh), Veratridine, Ionomycin or KCl had on the outflow of norepinephrine (NE) from lymphocytes was also studied. The effect of the addition of methoxyverapamil (D600, a Ca
2+ channel blocker) and cholinergic antagonists had on the ACh-induced NE outflow was assessed. CA were determined by HPLC–ECD, both in the supernatant and in the cell lysates.
l-Tyrosine and
l-Dopa significantly (
P<0.01) increased intracellular NE. Neither
l-tyrosine,
l-Dopa, nor vehicle induced a detectable outflow of NE to the supernatants. ACh [120
μM], Veratridine [100
μM], Ionomycin [10
μM] and KCl [50 mM] (with or without the simultaneous addition of
l-tyrosine or
l-Dopa) all induced a detectable outflow of NE to the supernatant when added 5 min before the end of incubation. NE was not detectable in the supernatant when the chemicals were added 10 to 20 min before the end of the incubation. When the chemicals were added at lower concentrations, erratic secretion or no secretion whatsoever was observed. D600 [100
μM] was able to significantly (
P<0.01) reduce the ACh-induced NE outflow. Tetraethylammonium (nicotinic antagonist), but not atropine (muscarinic antagonist), significantly (
P<0.001) decreased the ACh-induced NE outflow. The outflow of NE from peripheral human lymphocytes was seen. NE secretion seems to be ACh- and calcium-dependent since Veratridine, Ionomycin and KCl are able to induce Ca
2+ entry by means of various mechanisms. The Ca
2+ channel blocker employed in this study (D600) reduced the ACh-dependent NE outflow. We can conclude that both ACh (through nicotinic receptors) and calcium are involved in the outflow of NE from peripheral human lymphocytes.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>9670848</pmid><doi>10.1016/S0165-5728(98)00057-5</doi><tpages>6</tpages></addata></record> |
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| ispartof | Journal of neuroimmunology, 1998-07, Vol.87 (1), p.82-87 |
| issn | 0165-5728 1872-8421 |
| language | eng |
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| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | Acetylcholine Acetylcholine - pharmacology Adult Calcium Calcium - physiology Calcium Channel Blockers - pharmacology D600 Dose-Response Relationship, Drug Female Gallopamil - pharmacology Humans Ionomycin Ionomycin - pharmacology Levodopa - pharmacology Lymphocytes Lymphocytes - drug effects Lymphocytes - metabolism Male Norepinephrine Norepinephrine - metabolism Tyrosine - pharmacology Veratridine Veratridine - pharmacology |
| title | Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes |
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