Abstract：
:This study determined the contribution of cytochrome P450 (CP450) 4A enzyme metabolites of arachidonic acid in mediating the constriction of isolated rat skeletal muscle resistance arteries in response to elevated PO2. Gracilis arteries (GA) were viewed via television microscopy and constrictor responses to elevated PO2 were measured with a video micrometer. Endothelium removal and treatment of GA with 17-octadecynoic acid (17-ODYA; suicide substrate inhibitor of CP450 4A enzymes) impaired oxygen-induced constriction of the vessels; treatment of endothelium-denuded GA with 17-ODYA eliminated responses to elevated PO2. NOS inhibition and inhibition of EET production had no effect on oxygen-induced constriction of the vessels, although cyclooxygenase inhibition with indomethacin impaired GA responses to elevated PO2. Treatment of GA with dibromododecenyl methylsulfimide (DDMS; inhibitor of 20-hydroxyeicosatetraenoic acid (20-HETE) production) or 6(Z),15(Z)-20-HEDE (antagonist for 20-HETE receptors) mimicked the effects of 17-ODYA on GA responses to elevated PO2. Treatment of vessels with iberiotoxin or glibenclamide reduced the constriction of the vessels in response to elevated PO2 while treatment with both K+ channel blockers eliminated oxygen-induced constriction of the vessels. Following treatment of GA with indomethacin and 20-HETE, the vessels failed to respond to elevated PO2. These results suggest that oxygen-induced constriction of skeletal muscle resistance arteries represents the combined effects of reduced prostanoid release from the vascular endothelium and enhanced 20-HETE production in vascular smooth muscle cells.
journal_name
Microvasc Resjournal_title
Microvascular researchauthors
Frisbee JC,Krishna UM,Falck JR,Lombard JHdoi
10.1006/mvre.2001.2341keywords:
subject
Has Abstractpub_date
2001-11-01 00:00:00pages
271-83issue
3eissn
0026-2862issn
1095-9319pii
S0026-2862(01)92341-6journal_volume
62pub_type
杂志文章abstract：:We have applied theories of mass transfer, in laminar and turbulent flow, to red cells in the stopped-flow apparatus in order to estimate the effect of extracellular diffusion boundary layers on the initial rate of O2 uptake. We compared the theoretical predictions with the results of our previous stopped-flow experim...
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journal_title：Microvascular research
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journal_title：Microvascular research
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doi：10.1016/j.mvr.2004.11.001
更新日期：2005-01-01 00:00:00
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更新日期：2015-07-01 00:00:00
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更新日期：2012-03-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章
doi：10.1006/mvre.1998.2085
更新日期：1998-09-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章
doi：10.1006/mvre.1994.1028
更新日期：1994-05-01 00:00:00
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journal_title：Microvascular research
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doi：10.1006/mvre.1999.2224
更新日期：2000-03-01 00:00:00
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doi：10.1016/j.mvr.2006.03.001
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更新日期：2016-05-01 00:00:00
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pub_type： 杂志文章
doi：10.1016/0026-2862(83)90066-3
更新日期：1983-09-01 00:00:00
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doi：10.1016/j.mvr.2013.06.008
更新日期：2013-09-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章
doi：10.1006/mvre.1997.2067
更新日期：1998-03-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章
doi：10.1016/j.mvr.2009.12.001
更新日期：2010-03-01 00:00:00
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pub_type： 杂志文章
doi：10.1016/j.mvr.2019.04.009
更新日期：2019-09-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章
doi：10.1006/mvre.1995.1002
更新日期：1995-01-01 00:00:00
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journal_title：Microvascular research
pub_type： 杂志文章,随机对照试验
doi：10.1016/j.mvr.2010.10.001
更新日期：2011-01-01 00:00:00
