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Nitric oxide mediates arachidonic acid and prostaglandin E2‐ induced cerebral vasodilation independent of carbon monoxide
Author(s) -
Kanu Alie Joseph,
Leffler Charles W.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.685.19
Subject(s) - vasodilation , nitric oxide , arachidonic acid , chemistry , sodium nitroprusside , cerebral circulation , nitric oxide synthase , prostaglandin e2 , prostaglandin e , heme oxygenase , pharmacology , prostaglandin , endocrinology , anesthesia , medicine , biochemistry , heme , enzyme , organic chemistry
Nitric oxide mediates arachidonic acid and prostaglandin E2‐ induced cerebral vasodilation independent of carbon monoxide Carbon monoxide (CO) and nitric oxide (NO) are endogenously produced gaseous signaling molecules that can be involved in regulation of cerebral circulation. PGE 2 has been reported to increase NO production. Moreover, NO has been shown to be required as a permissive factor for CO‐induced cerebral vasodilation. NO also stimulates CO production in cerebral microvessels. Therefore, AA and PGE 2 generated in cerebral microvessels may increase cerebrovascular dilation either through NO or CO. In this study we tested this hypothesis by examining the effect of NO synthase inhibitors on the cerebrovascular response to AA and PGE 2 . Experiments were performed on anesthetized newborn pigs with closed cranial windows. In experiments with PGE 2 , indomethacin (5mg/kg i.v.) was administered to inhibit COX. Application of AA (10 −7 –10 −5 M) or PGE 2 (10 −7 10 −5 M) on cerebral vessels increased pial arteriolar diameter, which was blocked by both inhibitor of nitric oxide synthase, L‐NNA (1×10 −6 M) and heme oxygenase (HO) inhibitor chromium mesoporphyrin (CrMP) (2×10 −5 M). Sodium nitroprusside (SNP) (1×10 −9 –10 −6 M)‐induced cerebral vasodilation was not blocked by either L‐NNA or CrMP. These data suggest that NO mediated AA‐ and PGE 2 ‐induced cerebral vasodilation is independent of CO in newborn piglets.