Determination of seven prostanoids in 1 ml of urine by gas chromatography—negative ion chemical ionization triple stage quadrupole mass spectrometry

Schweer, Horst; Watzer, Bernhard; Seyberth, Hannsjörg W.

doi:10.1016/0378-4347(93)e0408-i

Cited by 71 publications

(51 citation statements)

References 22 publications

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“…To trigger the release of arachidonic acid from endogenous pools, cells were stimulated with 1 µM ionophore A23187 for 10 min. Thereafter the supernatants were stored at k20 mC until determination of the 6-oxo-PGF " α formed by GC-MS\MS as described previously [16]. Briefly, supernatant and deuterated reference substance were acidified to pH 3 with formic acid, and 1.5 M O-methylhydroxylamine hydrochloride was added to form the methoxime.…”

Section: Measurement Of the Conversion Of Arachidonic Acid From Endogmentioning

confidence: 99%

Effect of cyclic AMP and prostaglandin E2 on the induction of nitric oxide- and prostanoid-forming pathways in cultured rat mesangial cells

Nüsing

Klein

Pfeilschifter

et al. 1996

Biochemical Journal

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Cyclic AMP (cAMP) represents an important cellular signalling molecule. We analysed the effect of dibutyryl cAMP (db-cAMP), a cell-permeable and stable derivative of cAMP, on the regulation and expression of cyclo-oxygenase 2, inducible NO synthase and argininosuccinate synthetase. We observed different transcriptional regulation of these enzymes depending on the dbcAMP concentration used. Low concentrations of db-cAMP in the range 10-50 µM elevated levels of cyclo-oxygenase 2 mRNA, protein and activity, but not the respective mRNA and protein concentrations of the inducible NO synthase or argininosuccinate synthetase. At higher concentrations a massive induction of the

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Section: Measurement Of the Conversion Of Arachidonic Acid From Endogmentioning

confidence: 99%

Effect of cyclic AMP and prostaglandin E2 on the induction of nitric oxide- and prostanoid-forming pathways in cultured rat mesangial cells

Nüsing

Klein

Pfeilschifter

et al. 1996

Biochemical Journal

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“…In order to measure prostanoid concentrations, the hypothalamus was homogenized in 4 volumes of water (weight/volume) with an UltraTurrax and afterwards with a glass potter. Deuterated internal standards were added and prostanoids were extracted with 1 ml ethyl acetate/hexane (7:3, v/v) as described (Schweer et al, 1994). The sample was evaporated and reconstituted in 1 ml water.…”

Section: Methodsmentioning

confidence: 99%

“…The sample was evaporated and reconstituted in 1 ml water. Further derivatization and gas chromatography/triple quadrupole mass spectrometry (GC/MS/MS) conditions were described previously (Schweer et al, 1994).…”

Section: Methodsmentioning

confidence: 99%

“…The concentration of urinary prostacyclin metabolites (2,3-dinor-6-keto-prostaglandin F 1α and 6-ketoprostaglandin F 1α ) was determined by a commercial enzyme immunoassay kit (Assay Designs Inc., Ann Arbor, MI, USA). The concentration of the urinary PGE 2 metabolite 11α-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid was measured by GC/ MS/MS as described previously (Schweer et al, 1994). Urinary prostanoid concentrations were normalized with the concentration of creatinine, which was measured by the Metra creatinine assay kit (Quidel, San Diego, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

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Adaptation of the hypothalamic blood flow to chronic nitric oxide deficiency is independent of vasodilator prostanoids

et al. 2007

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The aim of our study was to investigate the adaptation of the hypothalamic circulation to chronic nitric oxide (NO) deficiency in rats. Hypothalamic blood flow (HBF) remained unaltered during chronic oral administration of the NO synthase (NOS) inhibitor N G -nitro-L-arginine methyl ester (L-NAME, 1 mg/ml drinking water) although acute NOS blockade by intravenous L-NAME injection (50 mg/kg) induced a dramatic HBF decrease. In chronically NOS blocked animals, however, acute L-NAME administration failed to influence the HBF. Reversal of chronic NOS blockade by intravenous L-arginine infusion evoked significant hypothalamic hyperemia suggesting the appearance of a compensatory vasodilator mechanism in the absence of NO. In order to clarify the potential involvement of vasodilator prostanoids in this adaptation, cyclooxygenase (COX) mRNA and protein levels were determined in the hypothalamus, but none of the known isoenzymes (COX-1, COX-2, COX-3) showed upregulation after chronic NOS blockade. Furthermore, levels of vasodilator prostanoid (PGI 2 , PGE 2 and PGD 2 ) metabolites were also not elevated. Interestingly, however, hypothalamic levels of vasoconstrictor prostanoids (TXA 2 and PGF 2α ) decreased after chronic NOS blockade. COX inhibition by indomethacin but not by diclofenac decreased the HBF in control animals. However, neither indomethacin nor diclofenac induced an altered HBF-response after chronic L-NAME treatment. Although urinary excretion of PGI 2 and PGE 2 metabolites markedly increased during chronic NOS blockade, indicating COX activation in the systemic circulation, we conclude that the adaptation of the hypothalamic circulation to the reduction of NO synthesis is independent of vasodilator prostanoids. Reduced release of vasoconstrictor prostanoids, however, may contribute to the normalization of HBF after chronic loss of NO.

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“…Prostanoid analyses were performed by gas chromatography-triple-stage quadrupole mass spectrometry (GC-MS-MS) according to previously published methods (Schweer et al 1994).…”

Section: Methodsmentioning

confidence: 99%

Dihydropyridmidinase deficiency and congenital microvillous atrophy: Coincidence or genetic relation?

Assmann

Hoffmann

Wagner

et al. 1997

J of Inher Metab Disea

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Determination of seven prostanoids in 1 ml of urine by gas chromatography—negative ion chemical ionization triple stage quadrupole mass spectrometry

Cited by 71 publications

References 22 publications

Effect of cyclic AMP and prostaglandin E2 on the induction of nitric oxide- and prostanoid-forming pathways in cultured rat mesangial cells

Effect of cyclic AMP and prostaglandin E2 on the induction of nitric oxide- and prostanoid-forming pathways in cultured rat mesangial cells

Adaptation of the hypothalamic blood flow to chronic nitric oxide deficiency is independent of vasodilator prostanoids

Dihydropyridmidinase deficiency and congenital microvillous atrophy: Coincidence or genetic relation?

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