Maternal and fetal nitric oxide production in normal and abnormal pregnancy.

Objectives: To characterize maternal and fetal nitric oxide (NO) production in normal and abnormal pregnancy by measuring nitrate (NO3-) and nitrite (NO2-) metabolites in maternal venous blood, umbilical venous and arterial blood and amniotic fluid.

Methods: This was a prospective cross-sectional study in 160 singleton pregnancies: 60 with one complication (infection, n = 37; gestational diabetes, n = 12; pre-eclampsia, n = 11) and 103 normal controls. Nitrate plus nitrite levels were assayed by reduction with Griess reagent.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-mediated membrane translocation of c-Src protein kinase in liver WB-F344 cells.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant and the most potent agonist of the aryl hydrocarbon receptor (AhR). Persistent activation of the AhR has been shown to be responsible for most TCDD-mediated toxic responses, including liver tumour promotion. However, the mechanisms responsible for these complex toxic reactions are still unknown.

Sympathetic sprouting: no evidence for muscarinic modulation of noradrenaline release in hippocampal slices of rats with fimbria-fornix lesions.

Lesions of the septohippocampal pathways elicit sprouting of sympathetic fibers from the superior cervical ganglion, a phenomenon which, within a few months, raises the hippocampal noradrenaline (NA) content above normal. In peripheral sympathetic fibers, the release of NA is modulated via presynaptic muscarinic receptors. Such receptors have not been detected so far on terminals of noradrenergic neurons originating in the locus coeruleus.

Daytime serum levels of melatonin after topical application onto the human skin.

The hormone melatonin is produced in the pineal gland and secreted into the blood in a circadian rhythm. Due to its antioxidative and immunomodulatory effects it might play a role as a topical drug in dermatology. In this study we investigated the penetration kinetics of melatonin applied to the skin of 6 healthy volunteers aged 26-34 years (M/F = 2/4).

Downregulation of muscarinic- and 5-HT1B-mediated modulation of [3H]acetylcholine release in hippocampal slices of rats with fimbria-fornix lesions and intrahippocampal grafts of septal origin.

Adult Long-Evans female rats sustained electrolytic fimbria-fornix lesions and, two weeks later, received intrahippocampal suspension grafts of fetal septal tissue. Sham-operated and lesion-only rats served as controls. Between 6.

3,4-Diaminopyridine-evoked noradrenaline release in rat hippocampal slices: facilitation by endogenous or exogenous nitric oxide.

The involvement of nitric oxide (NO) in the evoked release of noradrenaline (NA) was studied in rat hippocampal slices preincubated with [3H]NA and stimulated with 3,4-diaminopyridine (3,4-DAP; 200 microM) for 2 min. The 3,4-DAP-evoked [3H]overflow was enhanced by the NO synthase substrate L-arginine, but not by D-arginine; it was reduced by the NO synthase inhibitor NG-nitro-L-arginine, which also antagonized the effects of L-arginine. The corresponding nitro derivative of D-arginine was inactive and unable to block the effects of L-arginine.

Involvement of nitric oxide synthase in 3,4-diaminopyridine-evoked noradrenaline release in rat hippocampus.

The release of tritiated noradrenaline, evoked by stimulation of rat hippocampus slices with 3,4-diaminopyridine (200 microM, 2 min), was enhanced by the nitric oxide (NO) synthase substrate, L-arginine (but not by D-arginine), by NO donors (sodium nitroprusside, 3-morpholino-sydnonimine), and by 8-Br-cGMP. The effect of L-arginine was stereospecifically antagonized by NG-nitro-L-arginine, which given alone was inhibitory. From these findings we conclude that endogenously formed NO facilitates 3,4-diaminopyridine-evoked noradrenaline release in rat hippocampus.

Alpha 2-adrenoceptor mediated inhibition of exocytotic noradrenaline release in the absence of extracellular Ca2+.

The effect of the alpha 2-adrenoceptor agonist clonidine on 3,4-diaminopyridine (3,4-DAP)-evoked [3H]noradrenaline ([32H]NA) release in rat hippocampus slices was studied in the presence or absence (+1 mM EGTA) of extracellular Ca2+. 3H overflow (consisting mainly of unmetabolized [3H]NA) was evoked by addition of 100 microM 3,4-DAP for 10 min to the medium, which always contained 1 microM desipramine. Ligands for L-type voltage-sensitive Ca2+ channels (VSCC) did not affect the evoked [3H]NA release, whereas the preferential N-type VSCC antagonist omega-conotoxin was inhibitory, both in the presence and even more potently in the absence of Ca2+, suggesting an involvement of N-type VSCC in the mechanism of 3,4-DAP-evoked [3H]NA release.