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Article ; Online: Role of arachidonic acid lipoxygenase metabolites in the regulation of vascular tone.

Chawengsub, Yuttana / Gauthier, Kathryn M / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2009 Volume 297, Issue 2, Page(s) H495–507

Abstract: Stimulation of vascular endothelial cells with agonists such as acetylcholine (ACh) or bradykinin or with shear stress activates phospholipases and releases arachidonic acid (AA). AA is metabolized by cyclooxygenases, cytochrome P-450s, and lipoxygenases ...

Abstract	Stimulation of vascular endothelial cells with agonists such as acetylcholine (ACh) or bradykinin or with shear stress activates phospholipases and releases arachidonic acid (AA). AA is metabolized by cyclooxygenases, cytochrome P-450s, and lipoxygenases (LOs) to vasoactive products. In some arteries, a substantial component of the vasodilator response is dependent on LO metabolites of AA. Nitric oxide (NO)- and prostaglandin (PG)-independent vasodilatory responses to ACh and AA are reduced by inhibitors of LO and by antisense oligonucleotides specifically against 15-LO-1. Vasoactive 15-LO metabolites derived from the vascular endothelium include 15-hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-HEETA) that is hydrolyzed by soluble epoxide hydrolase to 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA). HEETA and THETA are endothelium-derived hyperpolarizing factors that induce vascular relaxations by activation of smooth muscle apamin-sensitive, calcium-activated, small-conductance K(+) channels causing hyperpolarization. In other arteries, the 12-LO metabolite 12-hydroxyeicosatetraenoic acid is synthesized by the vascular endothelium and relaxes smooth muscle by large-conductance, calcium-activated K(+) channel activation. Thus formation of vasodilator eicosanoids derived from LO pathways contributes to the regulation of vascular tone, local blood flow, and blood pressure.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/metabolism ; Animals ; Arachidonate 12-Lipoxygenase/metabolism ; Arachidonate 15-Lipoxygenase/metabolism ; Endothelium, Vascular/enzymology ; Humans ; Vasodilation/physiology
Chemical Substances	11,12,15-trihydroxyeicosatrienoic acid (82144-59-0) ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
Language	English
Publishing date	2009-06-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00349.2009
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Article: ACh-induced relaxations of rabbit small mesenteric arteries: role of arachidonic acid metabolites and K+.

Zhang, David X / Gauthier, Kathryn M / Chawengsub, Yuttana / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2007 Volume 293, Issue 1, Page(s) H152–9

Abstract: ACh-induced endothelium-dependent relaxation in rabbit small mesenteric arteries is resistant to N-nitro-L-arginine (L-NA) and indomethacin but sensitive to high K+, indicating the relaxations are mediated by endothelium-derived hyperpolarizing factors ( ... ...

Abstract	ACh-induced endothelium-dependent relaxation in rabbit small mesenteric arteries is resistant to N-nitro-L-arginine (L-NA) and indomethacin but sensitive to high K+, indicating the relaxations are mediated by endothelium-derived hyperpolarizing factors (EDHFs). The identity of the EDHFs in this vascular bed remains undefined. Small mesenteric arteries pretreated with L-NA and indomethacin were contracted with phenylephrine. ACh (10(-10) to 10(-6) M) caused concentration-dependent relaxations that were shifted to the right by lipoxygenase inhibition and the Ca(2+)-activated K+ channel inhibitors apamin (100 nM) or charybdotoxin (100 nM) and eliminated by the combination of apamin plus charybdotoxin. Relaxations to ACh were also blocked by a combination of barium (200 microM) and apamin but not barium plus charybdotoxin. Addition of K+ (10.9 mM final concentration) to the preconstricted arteries elicited small relaxations. K+ addition before ACh restored the charybdotoxin-sensitive component of relaxations to ACh. K+ (10.9 mM) also relaxed endothelium-denuded arteries, and the relaxations were inhibited by barium but not by charybdotoxin and apamin. With the use of whole cell patch-clamp analysis, ACh (10(-7) M) stimulated voltage-dependent outward K+ current from endothelial cells, which was inhibited by charybdotoxin, indicating K+ efflux. Arachidonic acid (10(-7) to 10(-4) M) induced concentration-related relaxations that were inhibited by apamin but not by charybdotoxin and barium. Addition of arachidonic acid after K+ (10.9 mM) resulted in more potent relaxations to arachidonic acid compared with control without K+ (5.9 mM). These findings suggest that, in rabbit mesenteric arteries, ACh-induced, L-NA- and indomethacin-resistant relaxation is mediated by endothelial cell K+ efflux and arachidonic acid metabolites, and a synergism exists between these two separate mechanisms.
MeSH term(s)	Acetylcholine/administration & dosage ; Animals ; Arachidonic Acid/metabolism ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Male ; Mesenteric Arteries/drug effects ; Mesenteric Arteries/physiology ; Potassium/metabolism ; Potassium Channel Blockers/administration & dosage ; Potassium Channels/drug effects ; Potassium Channels/physiology ; Rabbits ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Potassium Channel Blockers ; Potassium Channels ; Arachidonic Acid (27YG812J1I) ; Acetylcholine (N9YNS0M02X) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2007-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00268.2006
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Article: Structural characterization of monohydroxyeicosatetraenoic acids and dihydroxy- and trihydroxyeicosatrienoic acids by ESI-FTICR.

Cui, Lijie / Isbell, Marilyn A / Chawengsub, Yuttana / Falck, John R / Campbell, William B / Nithipatikom, Kasem

Journal of the American Society for Mass Spectrometry

2008 Volume 19, Issue 4, Page(s) 569–585

Abstract: The fragmentation characteristics of monohydroxyeicosatetraenoic acids and dihydroxy- and trihydroxyeicosatrienoic acids were investigated by electrospray ionization Fourier transform ion cyclotron resonance (FTICR) mass spectrometry using sustained off- ... ...

Abstract	The fragmentation characteristics of monohydroxyeicosatetraenoic acids and dihydroxy- and trihydroxyeicosatrienoic acids were investigated by electrospray ionization Fourier transform ion cyclotron resonance (FTICR) mass spectrometry using sustained off-resonance irradiation collision-induced dissociation (SORI-CID) and infrared multiphoton dissociation (IRMPD). The fragmentation patterns of these compounds were associated with the number and positions of the hydroxyl substituents. The fragmentation is more complicated with increasing number of the hydroxyl groups of the compounds. In general, the major carbon-carbon cleavage of [M - H](-) ions occurred at the alpha-position to the hydroxyl group, and the carbon-carbon cleavage occurred when there was a double-bond at the beta-position to the hydroxyl group. SORI-CID and IRMPD produced some common fragmentation patterns; however, each technique provided some unique patterns that are useful for structural identification of these compounds. This study demonstrated the application of FTICR via the identification of regioisomers of trihydroxyeicosatrienoic acids in rabbit aorta samples.
MeSH term(s)	Animals ; Animals, Newborn ; Aorta/chemistry ; Aorta/drug effects ; Aorta/metabolism ; Calcimycin/pharmacology ; Cyclotrons ; Hydroxyeicosatetraenoic Acids/chemistry ; Hydroxyl Radical/chemistry ; Indomethacin/pharmacology ; Rabbits ; Spectrometry, Mass, Electrospray Ionization/methods ; Spectroscopy, Fourier Transform Infrared/methods ; Tandem Mass Spectrometry
Chemical Substances	Hydroxyeicosatetraenoic Acids ; Hydroxyl Radical (3352-57-6) ; Calcimycin (37H9VM9WZL) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2008-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1073671-2
ISSN	1044-0305
ISSN	1044-0305
DOI	10.1016/j.jasms.2008.01.007
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Article: Identification of 13-Hydroxy-14,15-epoxyeicosatrienoic Acid as an Acid-stable Endothelium-derived Hyperpolarizing Factor in Rabbit Arteries

Chawengsub, Yuttana / Gauthier, Kathryn M / Nithipatikom, Kasem / Hammock, Bruce D / Falck, John R / Narsimhaswamy, Dubasi / Campbell, William B

Journal of biological chemistry. 2009 Nov. 6, v. 284, no. 45

2009

Abstract: Arachidonic acid (AA) is metabolized by endothelial 15-lipoxygenase (15-LO) to several vasodilatory eicosanoids such as 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA) and its proposed unstable precursor 15-hydroxy-11,12-epoxyeicosatrienoic acid ( ...

Abstract	Arachidonic acid (AA) is metabolized by endothelial 15-lipoxygenase (15-LO) to several vasodilatory eicosanoids such as 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA) and its proposed unstable precursor 15-hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-EETA). In the present study, the acid-stable 13-hydroxy-trans-14,15-epoxy-eicosatrienoic acid (13-H-14,15-EETA) was identified and its vascular activities characterized. Rabbit aorta, mesenteric arteries, and the combination of 15-LO and cytochrome P450 2J2 converted AA to two distinct HEETA metabolites. The HEETA metabolites were resistant to acidic hydrolysis but were hydrolyzed by recombinant sEH to a more polar metabolite identified by mass spectrometry as 13,14,15-THETA. Mass spectrometric analyses and HPLC comigration identified the HEETAs as threo- and erythro-diastereomers of 13-H-trans-14,15-EETA. Erythro- and threo-diastereomers of 13-H-trans-14,15-EETA relaxed endothelium-denuded rabbit small mesenteric arteries with maximum relaxations of 22.6 ± 6.0% and 8.6 ± 4.3%, respectively. Apamin (10⁻⁷ M) inhibited the relaxations to the erythro-isomer (maximum relaxation = 1.2 ± 5.6%) and increasing [K⁺]o from 4.6 to 30 mM blocked relaxations to both isomers. In cell-attached patches of mesenteric arterial smooth muscle cells (SMCs), erythro-13-H-trans-14,15-EETA (1-3 x 10⁻⁶ M) increased mean open time of small conductance K⁺ channels (13-14 pS) from 0.0007 ± 0.0007 to 0.0053 ± 0.0042. This activation was inhibited by apamin. The erythro, but not the threo, isomer blocked angiotensin II-stimulated aortic SMC migration. These studies demonstrate that 13-H-14,15-EETAs induces vascular relaxation via K⁺ channel activation to cause SMC hyperpolarization. Thus, 13-H-14,15-EETA represents a new endothelial factor.
Language	English
Dates of publication	2009-1106
Size	p. 31280-31290.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Role of arachidonic acid lipoxygenase metabolites in acetylcholine-induced relaxations of mouse arteries.

Gauthier, Kathryn M / Goldman, Daniel H / Aggarwal, Nitin T / Chawengsub, Yuttana / Falck, J R / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2010 Volume 300, Issue 3, Page(s) H725–35

Abstract: Arachidonic acid (AA) metabolites function as EDHFs in arteries of many species. They mediate cyclooxygenase (COX)- and nitric oxide (NO)-independent relaxations to acetylcholine (ACh). However, the role of AA metabolites as relaxing factors in mouse ... ...

Abstract	Arachidonic acid (AA) metabolites function as EDHFs in arteries of many species. They mediate cyclooxygenase (COX)- and nitric oxide (NO)-independent relaxations to acetylcholine (ACh). However, the role of AA metabolites as relaxing factors in mouse arteries remains incompletely defined. ACh caused concentration-dependent relaxations of the mouse thoracic and abdominal aorta and carotid, femoral, and mesentery arteries (maximal relaxation: 57 ± 4%, 72 ± 4%, 82 ± 3%, 80 ± 3%, and 85 ± 3%, respectively). The NO synthase inhibitor nitro-L-arginine (L-NA; 30 μM) blocked relaxations in the thoracic aorta, and L-NA plus the COX inhibitor indomethacin (10 μM) inhibited relaxations in the abdominal aorta and carotid, femoral, and mesenteric arteries (maximal relaxation: 31 ± 10%, 33 ± 5%, 41 ± 8%, and 73 ± 3%, respectively). In mesenteric arteries, NO- and COX-independent relaxations to ACh were inhibited by the lipoxygenase (LO) inhibitors nordihydroguaiaretic acid (NDGA; 10 μM) and BW-755C (200 μM), the K(+) channel inhibitor apamin (1 μM), and 60 mM KCl and eliminated by endothelium removal. They were not altered by the cytochrome P-450 inhibitor N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide (20 μM) or the epoxyeicosatrienoic acid antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (10 μM). AA relaxations were attenuated by NDGA or apamin and eliminated by 60 mM KCl. Reverse-phase HPLC analysis revealed arterial [(14)C]AA metabolites that comigrated with prostaglandins, trihydroxyeicosatrienoic acids (THETAs), hydroxyepoxyeicosatrienoic acids (HEETAs), and hydroxyeicosatetraenoic acids (HETEs). Epoxyeicosatrienoic acids were not observed. Mass spectrometry confirmed the identity of 6-keto-PGF(1α), PGE(2), 12-HETE, 15-HETE, HEETAs, 11,12,15-THETA, and 11,14,15-THETA. AA metabolism was blocked by NDGA and endothelium removal. 11(R),12(S),15(S)-THETA relaxations (maximal relaxation: 73 ± 3%) were endothelium independent and blocked by 60 mM KCl. Western immunoblot analysis and RT-PCR of the aorta and mesenteric arteries demonstrated protein and mRNA expression of leukocyte-type 12/15-LO. Thus, in mouse resistance arteries, 12/15-LO AA metabolites mediate endothelium-dependent relaxations to ACh and AA.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/pharmacology ; Acetylcholine/metabolism ; Amides/pharmacology ; Animals ; Apamin/pharmacology ; Arachidonate Lipoxygenases/metabolism ; Arteries/metabolism ; Arteries/physiopathology ; Female ; Indomethacin/pharmacology ; Male ; Masoprocol/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Nitroarginine/pharmacology ; Vasodilation/drug effects ; Vasodilator Agents/metabolism
Chemical Substances	Amides ; N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide ; Vasodilator Agents ; Nitroarginine (2149-70-4) ; Apamin (24345-16-2) ; Masoprocol (7BO8G1BYQU) ; 14,15-episulfide eicosatrienoic acid (98893-66-4) ; Arachidonate Lipoxygenases (EC 1.13.11.-) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S) ; Acetylcholine (N9YNS0M02X) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2010-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00696.2009
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Article ; Online: Identification of 13-hydroxy-14,15-epoxyeicosatrienoic acid as an acid-stable endothelium-derived hyperpolarizing factor in rabbit arteries.

Chawengsub, Yuttana / Gauthier, Kathryn M / Nithipatikom, Kasem / Hammock, Bruce D / Falck, John R / Narsimhaswamy, Dubasi / Campbell, William B

The Journal of biological chemistry

2009 Volume 284, Issue 45, Page(s) 31280–31290

Abstract	Arachidonic acid (AA) is metabolized by endothelial 15-lipoxygenase (15-LO) to several vasodilatory eicosanoids such as 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA) and its proposed unstable precursor 15-hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-EETA). In the present study, the acid-stable 13-hydroxy-trans-14,15-epoxy-eicosatrienoic acid (13-H-14,15-EETA) was identified and its vascular activities characterized. Rabbit aorta, mesenteric arteries, and the combination of 15-LO and cytochrome P450 2J2 converted AA to two distinct HEETA metabolites. The HEETA metabolites were resistant to acidic hydrolysis but were hydrolyzed by recombinant sEH to a more polar metabolite identified by mass spectrometry as 13,14,15-THETA. Mass spectrometric analyses and HPLC comigration identified the HEETAs as threo- and erythro-diastereomers of 13-H-trans-14,15-EETA. Erythro- and threo-diastereomers of 13-H-trans-14,15-EETA relaxed endothelium-denuded rabbit small mesenteric arteries with maximum relaxations of 22.6 +/- 6.0% and 8.6 +/- 4.3%, respectively. Apamin (10(-7) m) inhibited the relaxations to the erythro-isomer (maximum relaxation = 1.2 +/- 5.6%) and increasing [K(+)](o) from 4.6 to 30 mm blocked relaxations to both isomers. In cell-attached patches of mesenteric arterial smooth muscle cells (SMCs), erythro-13-H-trans-14,15-EETA (1-3 x 10(-6) m) increased mean open time of small conductance K(+) channels (13-14 pS) from 0.0007 +/- 0.0007 to 0.0053 +/- 0.0042. This activation was inhibited by apamin. The erythro, but not the threo, isomer blocked angiotensin II-stimulated aortic SMC migration. These studies demonstrate that 13-H-14,15-EETAs induces vascular relaxation via K(+) channel activation to cause SMC hyperpolarization. Thus, 13-H-14,15-EETA represents a new endothelial factor.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/chemistry ; 8,11,14-Eicosatrienoic Acid/metabolism ; Acids/pharmacology ; Animals ; Arachidonic Acid/metabolism ; Arteries/chemistry ; Arteries/cytology ; Arteries/drug effects ; Arteries/metabolism ; Endothelium, Vascular/chemistry ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; In Vitro Techniques ; Rabbits ; Vasodilator Agents/chemistry ; Vasodilator Agents/metabolism
Chemical Substances	Acids ; Vasodilator Agents ; Arachidonic Acid (27YG812J1I) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
Language	English
Publishing date	2009-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M109.025627
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Article: Chronic hypoxia enhances 15-lipoxygenase-mediated vasorelaxation in rabbit arteries.

Aggarwal, Nitin T / Pfister, Sandra L / Gauthier, Kathryn M / Chawengsub, Yuttana / Baker, John E / Campbell, William B

publication RETRACTED

American journal of physiology. Heart and circulatory physiology

2008 Volume 296, Issue 3, Page(s) H678–88

Abstract: 15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETAs) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial ...

Abstract	15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETAs) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial relaxations to agonists. We tested the effect of hypoxia on 15-LO-1 expression, THETA and HEETA synthesis, and relaxations in rabbit arteries. The incubation of rabbit aortic endothelial cells and isolated aortas in 0.7% O(2) increased 15-LO-1 expression. Rabbits were housed in a hypoxic atmosphere of 12% O(2) for 5 days. 15-LO-1 expression increased in the endothelium of the arteries of rabbits in 12% O(2) compared with room air. THETA and HEETA synthesis was also enhanced in aortas and mesenteric arteries. AA hyperpolarized the smooth muscle cells in indomethacin- and phenylephrine-treated mesenteric arteries of hypoxic rabbits from -29.4 +/- 1 to -50.1 +/- 3 mV. The hyperpolarization to AA was less in arteries of normoxic rabbits (from -26.0 +/- 2 to -37 +/- 2 mV). This AA-induced hyperpolarization was inhibited by the 15-LO inhibitor BW-755C. Nitric oxide and prostaglandin-independent maximum relaxations to acetylcholine (79.7 +/- 2%) and AA (38.3 +/- 4%) were enhanced in mesenteric arteries from hypoxic rabbits compared with the normoxic rabbits (49.7 +/- 6% and 19.9 +/- 2%, respectively). These relaxations were inhibited by BW-755C and nordihydroguaiaretic acid. Therefore, hypoxia increased the relaxations to agonists in the rabbit mesenteric arteries by enhancing endothelial 15-LO-1 expression and synthesis of the hyperpolarizing factors THETA and HEETA.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/metabolism ; Animals ; Arachidonate 15-Lipoxygenase/genetics ; Arachidonate 15-Lipoxygenase/metabolism ; Arachidonic Acid/metabolism ; Arteries/drug effects ; Arteries/enzymology ; Arteries/physiopathology ; Biological Factors/metabolism ; Cyclooxygenase Inhibitors/pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/physiopathology ; Hypoxia/enzymology ; Hypoxia/pathology ; Hypoxia/physiopathology ; Lipoxygenase Inhibitors/pharmacology ; Male ; Membrane Potentials ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/physiopathology ; Nitric Oxide/metabolism ; RNA, Messenger/metabolism ; Rabbits ; Time Factors ; Tunica Intima/pathology ; Vasoconstriction ; Vasoconstrictor Agents/pharmacology ; Vasodilation/drug effects ; Vasodilator Agents/pharmacology
Chemical Substances	15-hydroxy-11,12-epoxyeicosatrienoic acid ; Biological Factors ; Cyclooxygenase Inhibitors ; Lipoxygenase Inhibitors ; RNA, Messenger ; Vasoconstrictor Agents ; Vasodilator Agents ; endothelium-dependent hyperpolarization factor ; Arachidonic Acid (27YG812J1I) ; Nitric Oxide (31C4KY9ESH) ; 11,12,15-trihydroxyeicosatrienoic acid (82144-59-0) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
Language	English
Publishing date	2008-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Retracted Publication
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00777.2008
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Article: 11(R),12(S),15(S)-trihydroxyeicosa-5(Z),8(Z),13(E)-trienoic acid: an endothelium-derived 15-lipoxygenase metabolite that relaxes rabbit aorta.

Gauthier, Kathryn M / Chawengsub, Yuttana / Goldman, Daniel H / Conrow, Raymond E / Anjaiah, Siddam / Falck, J R / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2008 Volume 294, Issue 3, Page(s) H1467–72

Abstract: Previous studies indicate that 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA), an endothelium-derived hyperpolarizing factor in the rabbit aorta, mediates a portion of the relaxation response to acetylcholine by sequential metabolism of ... ...

Abstract	Previous studies indicate that 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA), an endothelium-derived hyperpolarizing factor in the rabbit aorta, mediates a portion of the relaxation response to acetylcholine by sequential metabolism of arachidonic acid by 15-lipoxygenase, hydroperoxide isomerase, and epoxide hydrolase. To determine the stereochemical configuration of the endothelial 11,12,15-THETA, its activity and chromatographic migration were compared with activity and migration of eight chemically synthesized stereoisomers of 11,12,15(S)-THETA. Of the eight isomers, only 11(R),12(S),15(S)-trihydroxyeicosa-5(Z),8(Z),13(E)-trienoic acid comigrated with the biological 11,12,15-THETA on reverse- and normal-phase HPLC and gas chromatography. The same THETA isomer (10(-7)-10(-4) M) relaxed the rabbit aorta in a concentration-related manner (maximum relaxation = 69 +/- 5%). These relaxations were blocked by apamin (10(-7) M), an inhibitor of small-conductance Ca2+-activated K+ channels. In comparison, 11(S),12(R),15(S),5(Z),8(Z),13(E)-THETA (10(-4) M) relaxed the aorta by 22%. The other six stereoisomers were inactive in this assay. With use of the whole cell patch-clamp technique, it was shown that 10(-4) M 11(R),12(S),15(S),5(Z),8(Z),13(E)-THETA increased outward K+ current in isolated aortic smooth muscle cells by 119 +/- 36% at +60 mV, whereas 10(-4) M 11(R),12(R),15(S),5(Z),8(Z),13(E)-THETA increased outward K+ current by only 20 +/- 2%. The 11(R),12(S),15(S),5(Z),8(Z),13(E)-THETA-stimulated increase in K+ current was blocked by pretreatment with apamin. These studies suggest that 11(R),12(S),15(S)-trihydroxyeicosa-5(Z),8(Z),13(E)-trienoic acid is the active stereoisomer produced by the rabbit aorta. It relaxes smooth muscle by activating K+ channels. The specific structural and stereochemical requirements for K+ channel activation suggest that a specific binding site or receptor of 11,12,15-THETA is involved in these actions.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/chemistry ; 8,11,14-Eicosatrienoic Acid/metabolism ; 8,11,14-Eicosatrienoic Acid/pharmacology ; Animals ; Aorta, Thoracic/drug effects ; Apamin/pharmacology ; Arachidonate 15-Lipoxygenase/metabolism ; Chromatography, High Pressure Liquid ; Data Interpretation, Statistical ; Endothelium, Vascular/metabolism ; Gas Chromatography-Mass Spectrometry ; In Vitro Techniques ; Isomerism ; Membrane Potentials/drug effects ; Muscle Relaxation/drug effects ; Muscle, Smooth, Vascular/drug effects ; Patch-Clamp Techniques ; Potassium Channel Blockers ; Potassium Channels/agonists ; Rabbits ; Stereoisomerism ; Vasodilator Agents/chemistry ; Vasodilator Agents/pharmacology
Chemical Substances	Potassium Channel Blockers ; Potassium Channels ; Vasodilator Agents ; Apamin (24345-16-2) ; 11,12,15-trihydroxyeicosatrienoic acid (82144-59-0) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
Language	English
Publishing date	2008-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.01052.2007
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Identification of 15-hydroxy-11,12-epoxyeicosatrienoic acid as a vasoactive 15-lipoxygenase metabolite in rabbit aorta.

Chawengsub, Yuttana / Aggarwal, Nitin T / Nithipatikom, Kasem / Gauthier, Kathryn M / Anjaiah, Siddam / Hammock, Bruce D / Falck, John R / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2008 Volume 294, Issue 3, Page(s) H1348–56

Abstract: Arachidonic acid (AA) causes endothelium-dependent smooth muscle hyperpolarizations and relaxations that are mediated by a 15-lipoxygenase-I (15-LO-I) metabolite, 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA). We propose that AA is metabolized ... ...

Abstract	Arachidonic acid (AA) causes endothelium-dependent smooth muscle hyperpolarizations and relaxations that are mediated by a 15-lipoxygenase-I (15-LO-I) metabolite, 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA). We propose that AA is metabolized sequentially by 15-LO-I and hydroperoxide isomerase to an unidentified hydroxyepoxyeicosatrienoic acid (HEETA), which is hydrolyzed by a soluble epoxide hydrolase (sEH) to 11,12,15-THETA. After incubation of aorta with 14C-labeled AA, metabolites were extracted and the HEETAs were resolved by performing HPLC. Mass spectrometric analyses identified 15-Hydroxy-11,12-epoxyeicosatrienoic acid (15-H-11,12-EETA). Incubation of aortic incubates with methanol and acetic acid trapped the acid-sensitive 15-H-11,12-EETA as methoxydihydroxyeicosatrienoic acids (MDHEs) (367 m/z, M-H). Pretreatment of the aortic tissue with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA; 10(-6) M) increased the formation of 15-H-11,12-EETA, measured as MDHEs. Thus 15-H-11,12-EETA is an acid- and sEH-sensitive precursor of 11,12,15-THETA. Aortic homogenates and endothelial cells contain a 57-kDa protein corresponding to the rabbit sEH. In preconstricted aortic rings, AA (10(-7)-10(-4) M) and acetylcholine (10(-9)-10(-6) M) caused concentration-related relaxations that were enhanced by pretreatment with AUDA. These enhanced relaxations were inhibited by increasing extracellular [K(+)] from 4.8 to 20 mM. AA (3 x 10(-6) M) induced cell membrane hyperpolarization (from -31.0 +/- 1 to -46.8 +/- 2 mV) in aortic strips with an intact endothelium, which was enhanced by AUDA. These results indicate that 15-H-11,12-EETA is produced by the aorta, hydrolyzed by sEH to 11,12,15-THETA, and mediates relaxations by membrane hyperpolarization. 15-H-11,12-EETA represents an endothelium-derived hyperpolarizing factor.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/chemistry ; 8,11,14-Eicosatrienoic Acid/metabolism ; Acetylcholine/metabolism ; Animals ; Aorta, Thoracic/metabolism ; Arachidonate 15-Lipoxygenase/metabolism ; Arachidonic Acids/metabolism ; Blotting, Western ; Chromatography, High Pressure Liquid ; Epoxide Hydrolases/metabolism ; Gas Chromatography-Mass Spectrometry ; Membrane Potentials/physiology ; Rabbits
Chemical Substances	15-hydroxy-11,12-epoxyeicosatrienoic acid ; Arachidonic Acids ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; Epoxide Hydrolases (EC 3.3.2.-) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S) ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2008-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.01326.2007
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Cyclooxygenase- and lipoxygenase-dependent relaxation to arachidonic acid in rabbit small mesenteric arteries.

Zhang, David X / Gauthier, Kathryn M / Chawengsub, Yuttana / Holmes, Blythe B / Campbell, William B

American journal of physiology. Heart and circulatory physiology

2004 Volume 288, Issue 1, Page(s) H302–9

Abstract: We recently reported that the lipoxygenase product 11,12,15-trihydroxyeicosatrienoic acid (THETA) mediates arachidonic acid (AA)-induced relaxation in the rabbit aorta. This study was designed to determine whether this lipoxygenase metabolite is involved ...

Abstract	We recently reported that the lipoxygenase product 11,12,15-trihydroxyeicosatrienoic acid (THETA) mediates arachidonic acid (AA)-induced relaxation in the rabbit aorta. This study was designed to determine whether this lipoxygenase metabolite is involved in relaxation responses to AA in rabbit small mesenteric arteries. AA (10(-9)-10(-4) M) produced potent relaxations in isolated phenylephrine-preconstricted arteries, with a maximal relaxation of 99 +/- 0.5% and EC(50) of 50 nM. The cyclooxygenase (COX) inhibitors indomethacin (10 microM), NS-398 (10 microM, selective for COX-2), and SC-560 (100 nM, selective for COX-1) caused a marked rightward shift of concentration responses to AA. With the use of immunohistochemical analysis, both COX-1 and COX-2 were detected in endothelium and smooth muscle of small mesenteric arteries. Indomethacin-resistant relaxations were further reduced by the lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-cyanocinnamate (CDC; 1 muM), nordihydroguaiaretic acid (NDGA; 1 microM), and ebselen (1 microM). HPLC analysis showed that [(14)C]AA was metabolized by mesenteric arteries to PGI(2), PGE(2), THETAs, hydroxyepoxyeicosatrienoic acids (HEETAs), and 15-hydroxyeicosatetraenoic acid (15-HETE). The production of PGI(2) and PGE(2) was blocked by indomethacin, and the production of THETAs, HEETAs, and 15-HETE was inhibited by CDC and NDGA. Column fractions corresponding to THETAs were further purified, analyzed by gas chromatography/mass spectrometry, and identified as 11,12,15- and 11,14,15-THETA. PGI(2), PGE(2), and purified THETA fractions relaxed mesenteric arteries precontracted with phenylephrine. The AA- and THETA-induced relaxations were blocked by high K(+) (60 mM). These findings provide functional and biochemical evidence that AA-induced relaxation in rabbit small mesenteric arteries is mediated through both COX and lipoxygenase pathways.
MeSH term(s)	Animals ; Arachidonic Acid/metabolism ; Arachidonic Acid/pharmacology ; Cyclooxygenase 1 ; Cyclooxygenase 2 ; In Vitro Techniques ; Lipoxygenase/physiology ; Male ; Mesenteric Arteries/drug effects ; Mesenteric Arteries/enzymology ; Mesenteric Arteries/physiology ; Prostaglandin-Endoperoxide Synthases/physiology ; Rabbits ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Arachidonic Acid (27YG812J1I) ; Lipoxygenase (EC 1.13.11.12) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2004-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00661.2004
Database	MEDical Literature Analysis and Retrieval System OnLINE

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