Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries
1. 1. In isolated goat middle cerebral artery segments, 5-hydroxytryptamine (5-HT, 10 −8−3 × 10 −5 M) caused concentration-dependent contractions, with EC 50 = 2.1 (1.9−2.5) × 10 −7 M and E max = 60 ± 2% of 50 mM KCl-induced contraction. 2. 2. Mechanical removal of endothelium significantly increase...
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| Veröffentlicht in: | General pharmacology 1993-05, Vol.24 (3), p.649-653 |
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| creator | Miranda, F.J. Torregrosa, G. Salom, J.B. Alabadí, J.A. Jover, T. Barberá, M.D. Alborch, E. |
| description | 1.
1. In isolated goat middle cerebral artery segments, 5-hydroxytryptamine (5-HT, 10
−8−3 × 10
−5 M) caused concentration-dependent contractions, with
EC
50 = 2.1 (1.9−2.5) × 10
−7 M and
E
max = 60 ± 2%
of 50 mM KCl-induced contraction.
2.
2. Mechanical removal of endothelium significantly increased the
E
max (91 ± 8%) and did not change the EC
50 value of 5-HT-elicited contractions.
3.
3. Incubation of unrubbed arteries with the irreversible inhibitor of EDRF, gossypol (10
−5 M), significantly increased the contractile response to 5-HT (
E
max = 77 ± 4%).
4.
4. Incubation of unrubbed arteries with the competitive inhibitor of the NO synthesis,
N
G-nitro
-
l-arginine
(L-NOARG) (10
−5 M), significantly enhanced the arterial response to 5-HT (
E
max = 71 ± 5%). The effects of L-NOARG were reversed by
l-arginine (10
−4 M) but not by
d-arginine (10
−4 M).
5.
5. Pretreatment with the inhibitor of cyclooxygenase, indomethacin (10
−5 M), significantly increased the response of unrubbed arteries to 5-HT, with an
E
max of 69 ± 3%.
6.
6. These results suggest that endothelium modulates the constrictor effect of 5-HT in goat cerebral arteries by producing both EDRF, probably NO, and prostacyclin. |
| doi_str_mv | 10.1016/0306-3623(93)90225-M |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_75945266</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>030636239390225M</els_id><sourcerecordid>75945266</sourcerecordid><originalsourceid>FETCH-LOGICAL-c452t-663080a6078c864147d9f7d4cf997395124428d7a497795a6343c931063ec1723</originalsourceid><addsrcrecordid>eNp9kE1LJDEQhoOsuOPs_gMX-rAseug1X510LsIifoGyF_e0hxCTao10J2OSFuff2-0McxQK6lBPvVU8CB0R_JtgIk4xw6JmgrJjxU4UprSp7_bQgrRS1RgT8gUtdshXdJjzM8aYNpQeoIOWiUZwsUD_L4KL5Ql6b_pqiG7sTfExVLGrmvpp7VJ8W5e0XhUz-AC1D2604CobQ0nGfqA-VI_RlMpCgoc0xZhUIHnI39B-Z_oM37d9if5dXtyfX9e3f69uzv_c1pY3tNRCMNxiI7BsbSs44dKpTjpuO6UkUw2hnNPWScOVlKoxgnFmFSNYMLBEUrZEvza5qxRfRshFDz5b6HsTII5Zy0ZNh6YzS8Q3oE0x5wSdXiU_mLTWBOvZqZ6F6VmYVlPNTvXdtPZjmz8-DOB2S1uJ0_zndm6yNX2XTLA-7zAuFSVqfvNsg8Hk4tVD0tl6CJNOn8AW7aL__I93GL-SAA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>75945266</pqid></control><display><type>article</type><title>Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Miranda, F.J. ; Torregrosa, G. ; Salom, J.B. ; Alabadí, J.A. ; Jover, T. ; Barberá, M.D. ; Alborch, E.</creator><creatorcontrib>Miranda, F.J. ; Torregrosa, G. ; Salom, J.B. ; Alabadí, J.A. ; Jover, T. ; Barberá, M.D. ; Alborch, E.</creatorcontrib><description>1.
1. In isolated goat middle cerebral artery segments, 5-hydroxytryptamine (5-HT, 10
−8−3 × 10
−5 M) caused concentration-dependent contractions, with
EC
50 = 2.1 (1.9−2.5) × 10
−7 M and
E
max = 60 ± 2%
of 50 mM KCl-induced contraction.
2.
2. Mechanical removal of endothelium significantly increased the
E
max (91 ± 8%) and did not change the EC
50 value of 5-HT-elicited contractions.
3.
3. Incubation of unrubbed arteries with the irreversible inhibitor of EDRF, gossypol (10
−5 M), significantly increased the contractile response to 5-HT (
E
max = 77 ± 4%).
4.
4. Incubation of unrubbed arteries with the competitive inhibitor of the NO synthesis,
N
G-nitro
-
l-arginine
(L-NOARG) (10
−5 M), significantly enhanced the arterial response to 5-HT (
E
max = 71 ± 5%). The effects of L-NOARG were reversed by
l-arginine (10
−4 M) but not by
d-arginine (10
−4 M).
5.
5. Pretreatment with the inhibitor of cyclooxygenase, indomethacin (10
−5 M), significantly increased the response of unrubbed arteries to 5-HT, with an
E
max of 69 ± 3%.
6.
6. These results suggest that endothelium modulates the constrictor effect of 5-HT in goat cerebral arteries by producing both EDRF, probably NO, and prostacyclin.</description><identifier>ISSN: 0306-3623</identifier><identifier>EISSN: 1879-0011</identifier><identifier>DOI: 10.1016/0306-3623(93)90225-M</identifier><identifier>PMID: 8365646</identifier><identifier>CODEN: GEPHDP</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Arginine - analogs & derivatives ; Arginine - pharmacology ; Biological and medical sciences ; Blood vessels and receptors ; Cerebral Arteries - drug effects ; Endothelium, Vascular - physiology ; Epoprostenol - pharmacology ; Female ; Fundamental and applied biological sciences. Psychology ; Goats ; Gossypol - pharmacology ; In Vitro Techniques ; Indomethacin - pharmacology ; Isometric Contraction - drug effects ; Muscle Contraction - drug effects ; Muscle, Smooth, Vascular - drug effects ; Nitric Oxide - pharmacology ; Nitroarginine ; Serotonin - pharmacology ; Vertebrates: cardiovascular system</subject><ispartof>General pharmacology, 1993-05, Vol.24 (3), p.649-653</ispartof><rights>1993</rights><rights>1993 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-663080a6078c864147d9f7d4cf997395124428d7a497795a6343c931063ec1723</citedby><cites>FETCH-LOGICAL-c452t-663080a6078c864147d9f7d4cf997395124428d7a497795a6343c931063ec1723</cites></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=4792192$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8365646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miranda, F.J.</creatorcontrib><creatorcontrib>Torregrosa, G.</creatorcontrib><creatorcontrib>Salom, J.B.</creatorcontrib><creatorcontrib>Alabadí, J.A.</creatorcontrib><creatorcontrib>Jover, T.</creatorcontrib><creatorcontrib>Barberá, M.D.</creatorcontrib><creatorcontrib>Alborch, E.</creatorcontrib><title>Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries</title><title>General pharmacology</title><addtitle>Gen Pharmacol</addtitle><description>1.
1. In isolated goat middle cerebral artery segments, 5-hydroxytryptamine (5-HT, 10
−8−3 × 10
−5 M) caused concentration-dependent contractions, with
EC
50 = 2.1 (1.9−2.5) × 10
−7 M and
E
max = 60 ± 2%
of 50 mM KCl-induced contraction.
2.
2. Mechanical removal of endothelium significantly increased the
E
max (91 ± 8%) and did not change the EC
50 value of 5-HT-elicited contractions.
3.
3. Incubation of unrubbed arteries with the irreversible inhibitor of EDRF, gossypol (10
−5 M), significantly increased the contractile response to 5-HT (
E
max = 77 ± 4%).
4.
4. Incubation of unrubbed arteries with the competitive inhibitor of the NO synthesis,
N
G-nitro
-
l-arginine
(L-NOARG) (10
−5 M), significantly enhanced the arterial response to 5-HT (
E
max = 71 ± 5%). The effects of L-NOARG were reversed by
l-arginine (10
−4 M) but not by
d-arginine (10
−4 M).
5.
5. Pretreatment with the inhibitor of cyclooxygenase, indomethacin (10
−5 M), significantly increased the response of unrubbed arteries to 5-HT, with an
E
max of 69 ± 3%.
6.
6. These results suggest that endothelium modulates the constrictor effect of 5-HT in goat cerebral arteries by producing both EDRF, probably NO, and prostacyclin.</description><subject>Animals</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>Cerebral Arteries - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Epoprostenol - pharmacology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Goats</subject><subject>Gossypol - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Indomethacin - pharmacology</subject><subject>Isometric Contraction - drug effects</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitroarginine</subject><subject>Serotonin - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><issn>0306-3623</issn><issn>1879-0011</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LJDEQhoOsuOPs_gMX-rAseug1X510LsIifoGyF_e0hxCTao10J2OSFuff2-0McxQK6lBPvVU8CB0R_JtgIk4xw6JmgrJjxU4UprSp7_bQgrRS1RgT8gUtdshXdJjzM8aYNpQeoIOWiUZwsUD_L4KL5Ql6b_pqiG7sTfExVLGrmvpp7VJ8W5e0XhUz-AC1D2604CobQ0nGfqA-VI_RlMpCgoc0xZhUIHnI39B-Z_oM37d9if5dXtyfX9e3f69uzv_c1pY3tNRCMNxiI7BsbSs44dKpTjpuO6UkUw2hnNPWScOVlKoxgnFmFSNYMLBEUrZEvza5qxRfRshFDz5b6HsTII5Zy0ZNh6YzS8Q3oE0x5wSdXiU_mLTWBOvZqZ6F6VmYVlPNTvXdtPZjmz8-DOB2S1uJ0_zndm6yNX2XTLA-7zAuFSVqfvNsg8Hk4tVD0tl6CJNOn8AW7aL__I93GL-SAA</recordid><startdate>19930501</startdate><enddate>19930501</enddate><creator>Miranda, F.J.</creator><creator>Torregrosa, G.</creator><creator>Salom, J.B.</creator><creator>Alabadí, J.A.</creator><creator>Jover, T.</creator><creator>Barberá, M.D.</creator><creator>Alborch, E.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>19930501</creationdate><title>Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries</title><author>Miranda, F.J. ; Torregrosa, G. ; Salom, J.B. ; Alabadí, J.A. ; Jover, T. ; Barberá, M.D. ; Alborch, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-663080a6078c864147d9f7d4cf997395124428d7a497795a6343c931063ec1723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>Cerebral Arteries - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Epoprostenol - pharmacology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Goats</topic><topic>Gossypol - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Indomethacin - pharmacology</topic><topic>Isometric Contraction - drug effects</topic><topic>Muscle Contraction - drug effects</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitroarginine</topic><topic>Serotonin - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>online_resources</toplevel><creatorcontrib>Miranda, F.J.</creatorcontrib><creatorcontrib>Torregrosa, G.</creatorcontrib><creatorcontrib>Salom, J.B.</creatorcontrib><creatorcontrib>Alabadí, J.A.</creatorcontrib><creatorcontrib>Jover, T.</creatorcontrib><creatorcontrib>Barberá, M.D.</creatorcontrib><creatorcontrib>Alborch, E.</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>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>General pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miranda, F.J.</au><au>Torregrosa, G.</au><au>Salom, J.B.</au><au>Alabadí, J.A.</au><au>Jover, T.</au><au>Barberá, M.D.</au><au>Alborch, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries</atitle><jtitle>General pharmacology</jtitle><addtitle>Gen Pharmacol</addtitle><date>1993-05-01</date><risdate>1993</risdate><volume>24</volume><issue>3</issue><spage>649</spage><epage>653</epage><pages>649-653</pages><issn>0306-3623</issn><eissn>1879-0011</eissn><coden>GEPHDP</coden><abstract>1.
1. In isolated goat middle cerebral artery segments, 5-hydroxytryptamine (5-HT, 10
−8−3 × 10
−5 M) caused concentration-dependent contractions, with
EC
50 = 2.1 (1.9−2.5) × 10
−7 M and
E
max = 60 ± 2%
of 50 mM KCl-induced contraction.
2.
2. Mechanical removal of endothelium significantly increased the
E
max (91 ± 8%) and did not change the EC
50 value of 5-HT-elicited contractions.
3.
3. Incubation of unrubbed arteries with the irreversible inhibitor of EDRF, gossypol (10
−5 M), significantly increased the contractile response to 5-HT (
E
max = 77 ± 4%).
4.
4. Incubation of unrubbed arteries with the competitive inhibitor of the NO synthesis,
N
G-nitro
-
l-arginine
(L-NOARG) (10
−5 M), significantly enhanced the arterial response to 5-HT (
E
max = 71 ± 5%). The effects of L-NOARG were reversed by
l-arginine (10
−4 M) but not by
d-arginine (10
−4 M).
5.
5. Pretreatment with the inhibitor of cyclooxygenase, indomethacin (10
−5 M), significantly increased the response of unrubbed arteries to 5-HT, with an
E
max of 69 ± 3%.
6.
6. These results suggest that endothelium modulates the constrictor effect of 5-HT in goat cerebral arteries by producing both EDRF, probably NO, and prostacyclin.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8365646</pmid><doi>10.1016/0306-3623(93)90225-M</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0306-3623 |
| ispartof | General pharmacology, 1993-05, Vol.24 (3), p.649-653 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Arginine - analogs & derivatives Arginine - pharmacology Biological and medical sciences Blood vessels and receptors Cerebral Arteries - drug effects Endothelium, Vascular - physiology Epoprostenol - pharmacology Female Fundamental and applied biological sciences. Psychology Goats Gossypol - pharmacology In Vitro Techniques Indomethacin - pharmacology Isometric Contraction - drug effects Muscle Contraction - drug effects Muscle, Smooth, Vascular - drug effects Nitric Oxide - pharmacology Nitroarginine Serotonin - pharmacology Vertebrates: cardiovascular system |
| title | Endothelial modulation of 5-hydroxytryptamine-induced contraction in goat cerebral arteries |
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