Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide
J. J. Marshall, E. P. Wei and H. A. Kontos Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298. We investigated the mechanisms of cerebral arteriolar dilation from topical acetylcholine and the nitrovasodilators, sodium nitroprusside, nitroglycerin,...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 1988-10, Vol.255 (4), p.H847-H854 |
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| container_issue | 4 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 255 |
| creator | Marshall, J. J Wei, E. P Kontos, H. A |
| description | J. J. Marshall, E. P. Wei and H. A. Kontos
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
We investigated the mechanisms of cerebral arteriolar dilation from topical
acetylcholine and the nitrovasodilators, sodium nitroprusside,
nitroglycerin, and nitric oxide, in anesthetized cats equipped with cranial
windows for the observation of the cerebral microcirculation.
Acetylcholine-mediated dilation was eliminated by topical methylene blue.
This blockade was reversed by either topical superoxide dismutase,
catalase, or deferoxamine. Nitroprusside- and nitric oxide-induced dilation
were not affected by methylene blue. Vasodilation from the
nitrovasodilators was significantly diminished by topical nitro blue
tetrazolium, but acetylcholine-mediated dilation was unaffected by nitro
blue tetrazolium. Neither methylene blue nor nitro blue tetrazolium
affected dilation from topical 8-bromoguanosine 3',5'-cyclic monophosphate.
These data show that methylene blue selectively blocks
acetylcholine-mediated endothelium-dependent dilation by generating oxygen
radicals. The mechanism involved is hydroxyl radical-mediated oxidation of
endothelium-derived relaxing factor. Nitro blue tetrazolium selectively
blocks dilation from the endothelium-independent nitrovasodilators. The
endothelium-derived relaxing factor generated by acetylcholine in the
cerebral microcirculation is not nitric oxide. |
| doi_str_mv | 10.1152/ajpheart.1988.255.4.H847 |
| format | Article |
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Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
We investigated the mechanisms of cerebral arteriolar dilation from topical
acetylcholine and the nitrovasodilators, sodium nitroprusside,
nitroglycerin, and nitric oxide, in anesthetized cats equipped with cranial
windows for the observation of the cerebral microcirculation.
Acetylcholine-mediated dilation was eliminated by topical methylene blue.
This blockade was reversed by either topical superoxide dismutase,
catalase, or deferoxamine. Nitroprusside- and nitric oxide-induced dilation
were not affected by methylene blue. Vasodilation from the
nitrovasodilators was significantly diminished by topical nitro blue
tetrazolium, but acetylcholine-mediated dilation was unaffected by nitro
blue tetrazolium. Neither methylene blue nor nitro blue tetrazolium
affected dilation from topical 8-bromoguanosine 3',5'-cyclic monophosphate.
These data show that methylene blue selectively blocks
acetylcholine-mediated endothelium-dependent dilation by generating oxygen
radicals. The mechanism involved is hydroxyl radical-mediated oxidation of
endothelium-derived relaxing factor. Nitro blue tetrazolium selectively
blocks dilation from the endothelium-independent nitrovasodilators. The
endothelium-derived relaxing factor generated by acetylcholine in the
cerebral microcirculation is not nitric oxide.</description><identifier>ISSN: 0363-6135</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.1988.255.4.H847</identifier><identifier>PMID: 2845816</identifier><language>eng</language><publisher>United States</publisher><subject>Acetylcholine - pharmacology ; Animals ; Arterioles - drug effects ; Arterioles - physiology ; Catalase - pharmacology ; Cats ; Cerebrovascular Circulation - drug effects ; Cyclic GMP - analogs & derivatives ; Cyclic GMP - pharmacology ; Deferoxamine - pharmacology ; Methylene Blue - pharmacology ; Nitric Oxide - pharmacology ; Nitroblue Tetrazolium - pharmacology ; Reference Values ; Superoxide Dismutase - pharmacology ; Vasodilation - drug effects</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 1988-10, Vol.255 (4), p.H847-H854</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c281t-fb03e386f457e3ae2c885a51f57dbdbad7af8b64a61fbf92063367c4158a67a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2845816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marshall, J. J</creatorcontrib><creatorcontrib>Wei, E. P</creatorcontrib><creatorcontrib>Kontos, H. A</creatorcontrib><title>Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol</addtitle><description>J. J. Marshall, E. P. Wei and H. A. Kontos
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
We investigated the mechanisms of cerebral arteriolar dilation from topical
acetylcholine and the nitrovasodilators, sodium nitroprusside,
nitroglycerin, and nitric oxide, in anesthetized cats equipped with cranial
windows for the observation of the cerebral microcirculation.
Acetylcholine-mediated dilation was eliminated by topical methylene blue.
This blockade was reversed by either topical superoxide dismutase,
catalase, or deferoxamine. Nitroprusside- and nitric oxide-induced dilation
were not affected by methylene blue. Vasodilation from the
nitrovasodilators was significantly diminished by topical nitro blue
tetrazolium, but acetylcholine-mediated dilation was unaffected by nitro
blue tetrazolium. Neither methylene blue nor nitro blue tetrazolium
affected dilation from topical 8-bromoguanosine 3',5'-cyclic monophosphate.
These data show that methylene blue selectively blocks
acetylcholine-mediated endothelium-dependent dilation by generating oxygen
radicals. The mechanism involved is hydroxyl radical-mediated oxidation of
endothelium-derived relaxing factor. Nitro blue tetrazolium selectively
blocks dilation from the endothelium-independent nitrovasodilators. The
endothelium-derived relaxing factor generated by acetylcholine in the
cerebral microcirculation is not nitric oxide.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - physiology</subject><subject>Catalase - pharmacology</subject><subject>Cats</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Cyclic GMP - analogs & derivatives</subject><subject>Cyclic GMP - pharmacology</subject><subject>Deferoxamine - pharmacology</subject><subject>Methylene Blue - pharmacology</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitroblue Tetrazolium - pharmacology</subject><subject>Reference Values</subject><subject>Superoxide Dismutase - pharmacology</subject><subject>Vasodilation - drug effects</subject><issn>0363-6135</issn><issn>0002-9513</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMtO3DAUhq2qFZ3SPgKSV90lxPElnmWFaAcJqarE3jqxj4nBE6d2Bpi3b0YzQDfnX_yXI32EUNbUjMn2Eh6mASHPNVtrXbdS1qLeaNF9IKvFbism-fojWTVc8UoxLj-TL6U8NE0jO8XPyFmrhdRMrcifm9HhhMsZZ9rHZB_BIU2eWszYZ4j0CUpyIcIc0kh9TlsKFud9tEOKYUQKo6NjmHOwNL0Eh1_JJw-x4LeTnpO7n9d3V5vq9vevm6sft5VtNZsr3zccuVZeyA45YGu1liCZl53rXQ-uA697JUAx3_t12yjOVWcFkxpUB_ycfD_OTjn93WGZzTYUizHCiGlXTKeFWnPRLkF9DNqcSsnozZTDFvLesMYcYJpXmOYA0ywwjTAHmEv14vRj12_RvRVP9Ba_PvpDuB-eQ0YzDfsSUkz3-_fV_wb_AYGLhVQ</recordid><startdate>19881001</startdate><enddate>19881001</enddate><creator>Marshall, J. J</creator><creator>Wei, E. P</creator><creator>Kontos, H. A</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><scope>7X8</scope></search><sort><creationdate>19881001</creationdate><title>Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide</title><author>Marshall, J. J ; Wei, E. P ; Kontos, H. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c281t-fb03e386f457e3ae2c885a51f57dbdbad7af8b64a61fbf92063367c4158a67a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - physiology</topic><topic>Catalase - pharmacology</topic><topic>Cats</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Cyclic GMP - analogs & derivatives</topic><topic>Cyclic GMP - pharmacology</topic><topic>Deferoxamine - pharmacology</topic><topic>Methylene Blue - pharmacology</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitroblue Tetrazolium - pharmacology</topic><topic>Reference Values</topic><topic>Superoxide Dismutase - pharmacology</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marshall, J. J</creatorcontrib><creatorcontrib>Wei, E. P</creatorcontrib><creatorcontrib>Kontos, H. A</creatorcontrib><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>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marshall, J. J</au><au>Wei, E. P</au><au>Kontos, H. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1988-10-01</date><risdate>1988</risdate><volume>255</volume><issue>4</issue><spage>H847</spage><epage>H854</epage><pages>H847-H854</pages><issn>0363-6135</issn><issn>0002-9513</issn><eissn>1522-1539</eissn><abstract>J. J. Marshall, E. P. Wei and H. A. Kontos
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
We investigated the mechanisms of cerebral arteriolar dilation from topical
acetylcholine and the nitrovasodilators, sodium nitroprusside,
nitroglycerin, and nitric oxide, in anesthetized cats equipped with cranial
windows for the observation of the cerebral microcirculation.
Acetylcholine-mediated dilation was eliminated by topical methylene blue.
This blockade was reversed by either topical superoxide dismutase,
catalase, or deferoxamine. Nitroprusside- and nitric oxide-induced dilation
were not affected by methylene blue. Vasodilation from the
nitrovasodilators was significantly diminished by topical nitro blue
tetrazolium, but acetylcholine-mediated dilation was unaffected by nitro
blue tetrazolium. Neither methylene blue nor nitro blue tetrazolium
affected dilation from topical 8-bromoguanosine 3',5'-cyclic monophosphate.
These data show that methylene blue selectively blocks
acetylcholine-mediated endothelium-dependent dilation by generating oxygen
radicals. The mechanism involved is hydroxyl radical-mediated oxidation of
endothelium-derived relaxing factor. Nitro blue tetrazolium selectively
blocks dilation from the endothelium-independent nitrovasodilators. The
endothelium-derived relaxing factor generated by acetylcholine in the
cerebral microcirculation is not nitric oxide.</abstract><cop>United States</cop><pmid>2845816</pmid><doi>10.1152/ajpheart.1988.255.4.H847</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 1988-10, Vol.255 (4), p.H847-H854 |
| issn | 0363-6135 0002-9513 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_255_4_H847 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Animals Arterioles - drug effects Arterioles - physiology Catalase - pharmacology Cats Cerebrovascular Circulation - drug effects Cyclic GMP - analogs & derivatives Cyclic GMP - pharmacology Deferoxamine - pharmacology Methylene Blue - pharmacology Nitric Oxide - pharmacology Nitroblue Tetrazolium - pharmacology Reference Values Superoxide Dismutase - pharmacology Vasodilation - drug effects |
| title | Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide |
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