Indomethacin-sensitive CO2 reactivity of cerebral arterioles is restored by vasodilator prostaglandin
L. C. Wagerle and P. A. Degiulio Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104. To investigate the role of vasodilator prostanoids in the CO2-induced relaxation of cerebral arterioles, the present study examined the effect of exogenous prostaglandin (PG)...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 1994-04, Vol.266 (4), p.H1332-H1338 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
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| creator | Wagerle, L. C Degiulio, P. A |
| description | L. C. Wagerle and P. A. Degiulio
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
To investigate the role of vasodilator prostanoids in the CO2-induced
relaxation of cerebral arterioles, the present study examined the effect of
exogenous prostaglandin (PG) E2 and nonprostanoid vasodilators, adenosine
and sodium nitroprusside, on the indomethacin-impaired pial arteriolar
response to CO2 in newborn piglets. Reactivity of pial arterioles (52-131
microns diam) was determined using a closed cranial window with intravital
microscopy. Cortical prostanoid synthesis was assessed by analyzing for
select prostanoids in cerebrospinal fluid sampled from under the cranial
window. Inhalation of 7% CO2 caused an elevation of cortical 6-keto-PGF1
alpha and thromboxane (Tx) B2 and increased pial arteriolar diameter by 34
+/- 5%. Two cyclooxygenase inhibitors, indomethacin (5 mg/kg i.v.) and
ibuprofen (30 mg/kg i.v.), abolished the CO2-induced elevation of cortical
prostanoids. Indomethacin, but not ibuprofen, blocked the CO2-induced
increase in pial arteriolar diameter. The indomethacin-impaired vasodilator
response to CO2 was restored when PGE2 (0.1-1 microM) was applied topically
to the cortical surface. Adenosine (1-100 microM) and sodium nitroprusside
(0.5 microM) only partially restored the vasodilator response to CO2. The
data suggest that vasodilator prostanoids facilitate cerebrovascular
relaxation to CO2 and may play a permissive role in the relaxation response
of vascular smooth muscle. The fact that adenosine (adenosine 3',5'-cyclic
monophosphate-mediated dilator) and sodium nitroprusside (guanosine
3',5'-cyclic monophosphate-mediated dilator), were partially effective
suggests a role for those intracellular signaling pathways. We speculate
that receptor activation of intracellular pathways may alter Ca2+
sensitivity of the contractile apparatus in such a way that the relaxation
response to CO2 can occur. |
| doi_str_mv | 10.1152/ajpheart.1994.266.4.H1332 |
| format | Article |
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Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
To investigate the role of vasodilator prostanoids in the CO2-induced
relaxation of cerebral arterioles, the present study examined the effect of
exogenous prostaglandin (PG) E2 and nonprostanoid vasodilators, adenosine
and sodium nitroprusside, on the indomethacin-impaired pial arteriolar
response to CO2 in newborn piglets. Reactivity of pial arterioles (52-131
microns diam) was determined using a closed cranial window with intravital
microscopy. Cortical prostanoid synthesis was assessed by analyzing for
select prostanoids in cerebrospinal fluid sampled from under the cranial
window. Inhalation of 7% CO2 caused an elevation of cortical 6-keto-PGF1
alpha and thromboxane (Tx) B2 and increased pial arteriolar diameter by 34
+/- 5%. Two cyclooxygenase inhibitors, indomethacin (5 mg/kg i.v.) and
ibuprofen (30 mg/kg i.v.), abolished the CO2-induced elevation of cortical
prostanoids. Indomethacin, but not ibuprofen, blocked the CO2-induced
increase in pial arteriolar diameter. The indomethacin-impaired vasodilator
response to CO2 was restored when PGE2 (0.1-1 microM) was applied topically
to the cortical surface. Adenosine (1-100 microM) and sodium nitroprusside
(0.5 microM) only partially restored the vasodilator response to CO2. The
data suggest that vasodilator prostanoids facilitate cerebrovascular
relaxation to CO2 and may play a permissive role in the relaxation response
of vascular smooth muscle. The fact that adenosine (adenosine 3',5'-cyclic
monophosphate-mediated dilator) and sodium nitroprusside (guanosine
3',5'-cyclic monophosphate-mediated dilator), were partially effective
suggests a role for those intracellular signaling pathways. We speculate
that receptor activation of intracellular pathways may alter Ca2+
sensitivity of the contractile apparatus in such a way that the relaxation
response to CO2 can occur.</description><identifier>ISSN: 0363-6135</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.1994.266.4.H1332</identifier><identifier>PMID: 8184911</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Animals, Newborn ; Arterioles - drug effects ; Carbon Dioxide - pharmacology ; Cerebrovascular Circulation - drug effects ; Ibuprofen - pharmacology ; Indomethacin - pharmacology ; Pia Mater - blood supply ; Prostaglandins - biosynthesis ; Prostaglandins - pharmacology ; Swine ; Vasodilator Agents - pharmacology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 1994-04, Vol.266 (4), p.H1332-H1338</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-5fb3ed69eecb186b10a2bd97fb5e41bd5d9502de900a62bcc535cb0048619c1d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8184911$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wagerle, L. C</creatorcontrib><creatorcontrib>Degiulio, P. A</creatorcontrib><title>Indomethacin-sensitive CO2 reactivity of cerebral arterioles is restored by vasodilator prostaglandin</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol</addtitle><description>L. C. Wagerle and P. A. Degiulio
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
To investigate the role of vasodilator prostanoids in the CO2-induced
relaxation of cerebral arterioles, the present study examined the effect of
exogenous prostaglandin (PG) E2 and nonprostanoid vasodilators, adenosine
and sodium nitroprusside, on the indomethacin-impaired pial arteriolar
response to CO2 in newborn piglets. Reactivity of pial arterioles (52-131
microns diam) was determined using a closed cranial window with intravital
microscopy. Cortical prostanoid synthesis was assessed by analyzing for
select prostanoids in cerebrospinal fluid sampled from under the cranial
window. Inhalation of 7% CO2 caused an elevation of cortical 6-keto-PGF1
alpha and thromboxane (Tx) B2 and increased pial arteriolar diameter by 34
+/- 5%. Two cyclooxygenase inhibitors, indomethacin (5 mg/kg i.v.) and
ibuprofen (30 mg/kg i.v.), abolished the CO2-induced elevation of cortical
prostanoids. Indomethacin, but not ibuprofen, blocked the CO2-induced
increase in pial arteriolar diameter. The indomethacin-impaired vasodilator
response to CO2 was restored when PGE2 (0.1-1 microM) was applied topically
to the cortical surface. Adenosine (1-100 microM) and sodium nitroprusside
(0.5 microM) only partially restored the vasodilator response to CO2. The
data suggest that vasodilator prostanoids facilitate cerebrovascular
relaxation to CO2 and may play a permissive role in the relaxation response
of vascular smooth muscle. The fact that adenosine (adenosine 3',5'-cyclic
monophosphate-mediated dilator) and sodium nitroprusside (guanosine
3',5'-cyclic monophosphate-mediated dilator), were partially effective
suggests a role for those intracellular signaling pathways. We speculate
that receptor activation of intracellular pathways may alter Ca2+
sensitivity of the contractile apparatus in such a way that the relaxation
response to CO2 can occur.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Arterioles - drug effects</subject><subject>Carbon Dioxide - pharmacology</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Ibuprofen - pharmacology</subject><subject>Indomethacin - pharmacology</subject><subject>Pia Mater - blood supply</subject><subject>Prostaglandins - biosynthesis</subject><subject>Prostaglandins - pharmacology</subject><subject>Swine</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0363-6135</issn><issn>0002-9513</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkM1u2zAQhIkiReKkfYQC7CU3KVxSpM1jYTR1gAC5tGeCPyuLgSw5pJxCbx-6dpueiOXMziw-Qr4CqwEkv7PP-w5tmmrQuqm5UnVTb0AI_oEsis4rkEJfkAUTSlQKhLwi1zk_M8bkUolLcrmCVaMBFgQfhjDucOqsj0OVcchxiq9I10-cJrS-DHGa6dhSjwldsj0tvZji2GOmMRdTnsaEgbqZvto8htjb8kH3acyT3fZ2CHH4RD62ts_4-fzekF_333-uN9Xj04-H9bfHygvJp0q2TmBQGtE7WCkHzHIX9LJ1EhtwQQYtGQ-oGbOKO--lkN4x1qwUaA9B3JDbU25pfzmUy8wuZo99uQLHQzZLdbQCFKM-GX05MydszT7FnU2zAWaOiM1fxOaI2BTEpjF_EJfdL-eSg9th-Ld5Zlr0u5PexW33OyY0-27OBdi4nd9j_098A1nqjiQ</recordid><startdate>19940401</startdate><enddate>19940401</enddate><creator>Wagerle, L. C</creator><creator>Degiulio, P. 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>19940401</creationdate><title>Indomethacin-sensitive CO2 reactivity of cerebral arterioles is restored by vasodilator prostaglandin</title><author>Wagerle, L. C ; Degiulio, P. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-5fb3ed69eecb186b10a2bd97fb5e41bd5d9502de900a62bcc535cb0048619c1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Arterioles - drug effects</topic><topic>Carbon Dioxide - pharmacology</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Ibuprofen - pharmacology</topic><topic>Indomethacin - pharmacology</topic><topic>Pia Mater - blood supply</topic><topic>Prostaglandins - biosynthesis</topic><topic>Prostaglandins - pharmacology</topic><topic>Swine</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wagerle, L. C</creatorcontrib><creatorcontrib>Degiulio, P. 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>Wagerle, L. C</au><au>Degiulio, P. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Indomethacin-sensitive CO2 reactivity of cerebral arterioles is restored by vasodilator prostaglandin</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1994-04-01</date><risdate>1994</risdate><volume>266</volume><issue>4</issue><spage>H1332</spage><epage>H1338</epage><pages>H1332-H1338</pages><issn>0363-6135</issn><issn>0002-9513</issn><eissn>1522-1539</eissn><abstract>L. C. Wagerle and P. A. Degiulio
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
To investigate the role of vasodilator prostanoids in the CO2-induced
relaxation of cerebral arterioles, the present study examined the effect of
exogenous prostaglandin (PG) E2 and nonprostanoid vasodilators, adenosine
and sodium nitroprusside, on the indomethacin-impaired pial arteriolar
response to CO2 in newborn piglets. Reactivity of pial arterioles (52-131
microns diam) was determined using a closed cranial window with intravital
microscopy. Cortical prostanoid synthesis was assessed by analyzing for
select prostanoids in cerebrospinal fluid sampled from under the cranial
window. Inhalation of 7% CO2 caused an elevation of cortical 6-keto-PGF1
alpha and thromboxane (Tx) B2 and increased pial arteriolar diameter by 34
+/- 5%. Two cyclooxygenase inhibitors, indomethacin (5 mg/kg i.v.) and
ibuprofen (30 mg/kg i.v.), abolished the CO2-induced elevation of cortical
prostanoids. Indomethacin, but not ibuprofen, blocked the CO2-induced
increase in pial arteriolar diameter. The indomethacin-impaired vasodilator
response to CO2 was restored when PGE2 (0.1-1 microM) was applied topically
to the cortical surface. Adenosine (1-100 microM) and sodium nitroprusside
(0.5 microM) only partially restored the vasodilator response to CO2. The
data suggest that vasodilator prostanoids facilitate cerebrovascular
relaxation to CO2 and may play a permissive role in the relaxation response
of vascular smooth muscle. The fact that adenosine (adenosine 3',5'-cyclic
monophosphate-mediated dilator) and sodium nitroprusside (guanosine
3',5'-cyclic monophosphate-mediated dilator), were partially effective
suggests a role for those intracellular signaling pathways. We speculate
that receptor activation of intracellular pathways may alter Ca2+
sensitivity of the contractile apparatus in such a way that the relaxation
response to CO2 can occur.</abstract><cop>United States</cop><pmid>8184911</pmid><doi>10.1152/ajpheart.1994.266.4.H1332</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 1994-04, Vol.266 (4), p.H1332-H1338 |
| issn | 0363-6135 0002-9513 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_266_4_H1332 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Animals, Newborn Arterioles - drug effects Carbon Dioxide - pharmacology Cerebrovascular Circulation - drug effects Ibuprofen - pharmacology Indomethacin - pharmacology Pia Mater - blood supply Prostaglandins - biosynthesis Prostaglandins - pharmacology Swine Vasodilator Agents - pharmacology |
| title | Indomethacin-sensitive CO2 reactivity of cerebral arterioles is restored by vasodilator prostaglandin |
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