Assessment of superoxide-mediated release of vascular-inhibitory factor(s) from endothelial cells by using a two-bath system

Summary Release of a vascular-inhibitory factor from endothelial cells (EC), different from endothelium-derived relaxant factor (EDRF), was identified through use of a two-bath system. This two-bath system precluded the effects of oxygen-free radicals that appear when electrical field stimulation (EFS) is directly imposed on detector muscle.     

Chronic sensory denervation reduces thrombin-stimulated endothelin release from aortic endothelial cells

The long-term (trophic) influence of perivascular nerves on the endothelium was investigated by measuring changes in thrombin-stimulated release of the potent vasoconstrictor, endothelin, after selective chronic denervation. Rat pups were treated with either guanethidine or capsaicin to destroy sympathetic or sensory nerves, respectively. The abdominal aortas from the rats at three months of age (5 pooled per experiment) were incubated with 4U thrombin/ml in medium for 24 h at 37°C, and the amount of endothelin released from the preparation determined by immunoassay. After neonatal sensory denervation there was a significant reduction in the thrombinstimulated release of endothelin compared to the controls (0.012±0.012 (4) compared to 0.063±0.012 (6), pmol/cm²/24 h, p<0.02). There was no change in endothelin release after sympathetic denervation. In summary, sensory nerves play a trophic role in the expression of endothelin in endothelial cells of the intima.     

Synergistic effect of acute hypoxia on flow-induced release of ATP from cultured endothelial cells

Human umbilical vein endothelial cells (HUVECs) in primary cultures were perfused under normoxic or hypoxic conditions. These cells were stimulated twice for 3 min by increased flow (from 0.5 to 3.0 ml/min). Under hypoxic conditions the basal release of ATP was the same as under normoxic conditions, but during increased flow the release was greater (0.58±0.07>0.32±0.04 pmoles/ml/10⁶ cells (+78%), for the first period of stimulation; 0.39±0.05>0.22±0.03 pmoles/ml/10⁶ cells (+79%) for the second period). Further experiments with sequential increments in flow rate showed that under both normoxic and hypoxic conditions, a positive correlation existed between ATP release and the rate of flow but there was always more ATP released under hypoxic conditions regardless of the flow rate.HUVECs in secondary culture (second passage) were similarly stimulated. No differences were observed between normoxic and hypoxic conditions. In both cases, the quantity of ATP released during high flow (0.050±0.004 pmoles/ml/10⁶ cells) was significantly smaller than the quantity of ATP released during low flow (0.09±0.01 pmoles/ml/10⁶ cells).To conclude, since hypoxia alone did not affect ATP release, there appears to be a synergistic relationship between increased shear stress and hypoxia in the stimulation of ATP release from HUVECs. Moreover, the release of ATP under these conditions seems to be a property of highly differentiated endothelial cells.     

The power of VEGF (vascular endothelial growth factor) family molecules

Vascular endothelial growth factors (VEGFs) and their high-affinity tyrosine kinase VEGF receptors (VEGFRs) are key regulators of both angiogenesis and neurogenesis. The current issue of CMLS discusses recent literature and work implementing these signals in nervous system development, maintenance and disease pathology.     

Flow-induced release of adenosine 5'-triphosphate from endothelial cells of the rat mesenteric arterial bed.

Adenosine 5'-triphosphate (ATP) was released into the perfusate of rat isolated mesenteric arterial beds during each of two consecutive increases in flow. There was no significant difference between the amounts of ATP released on each occasion. Substance P was also released into the perfusate by increased flow, although its release was more variable. Removal of the endothelium of the mesenteric vessels with sodium deoxycholate led to a significant reduction (74%) in the amount of ATP released compared with the release before the endothelium had been removed. This suggests that the ATP released into the mesenteric arterial perfusate during increased flow arises from endothelial cells.     

Increase in activity of natural killer cells (NK cells) by serum thymic factor]

The serum thymic factor (FTS) and one of its structural analogues have been administered to adult normal Mice for 2 to 12 weeks. This treatment induced a significant increase in spleen cell natural killer (NK) activity, evaluated by a cytotoxicity assay against YAC cells.     

Studies on antithiamine factor(s) in tissue of tuna and goatfish

Zusammenfassung Es wurden Antithiaminwirkstoffe bei Hawaii-Fischen untersucht und gezeigt, dass die Antithiaminaktivität nicht enzymatisch ist.

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This investigation was supported in part by Public Health Service Research Grant No. AM-8531.     

Endothelial cells as part of a vascular oxygen-sensing system: hypoxia-induced release of autacoids

Higher developed organisms are equipped with many central and local control mechanisms, which enable an adequate blood and oxygen supply to tissues over a wide range of demands. Global adaptive responses include changes in the circulatory and ventilatory system as well as increases in the oxygen carrying capacity of the blood. At the level of the specialized organs there exist additional control systems for the regulation of local blood flow. Most systems make use of highly specialized cells which are able to sense the oxygen partial pressure of the transport medium, blood, and within the tissues. In the past years, it has been shown that the vascular endothelium lining the entire circulatory system can actively modulate the vascular tone and platelet functions by the release of autacoids, among them prostacyclin and endothelium-derived nitric oxide (EDRF). Recent experiments demonstrate that the release of EDRF is PO2-dependent, which suggests that endothelial cells may act as functional local oxygen sensors within the vascular system.     

Inflamed-tissue factor(s): An autoregulatory mechanism of some acute inflammatory responses

Zusammenfassung Bei Ratten wurde aus entzündetem Gewebe ein Hemmer für das Komplementsystem extrahiert, welcher die durch Carrageenin oder Kaolin erzeugten Entzündungen zu unterdrücken vermag.     

Failure to identify ‘thrombocytolysin’ (a spasmogenic factor released from platelets by immunoreaction) with anaphylatoxin

Summary Horse platelets release an unidentified smooth muscle contracting substance after lysis by antiserum and complement. Since the active factor (thrombocytolysin) does not produce tachyphylactic response of the guinea-pig ileum it seems that it is not related to anaphylatoxins.     

Retroviruses released from a human tumor xenograft in nude mice induce colony-stimulating factor (CSF) activity in human fibroblastic cells

Summary A human colony-stimulating factor (CSF)-producing tumor transplanted into athymic nude mice released retroviruses in vitro. The viruses induced CSF activity in human fibroblastic cell lines.     

Retroviruses released from a human tumor xenograft in nude mice induce colony-stimulating factor (CSF) activity in human fibroblastic cells

A human colony-stimulating factor (CSF)-producing tumor transplanted into athymic nude mice released retroviruses in vitro. The viruses induced CSF activity in human fibroblastic cell lines.     

Purification of plasminogen activator(s) from human seminal plasma

Summary Human seminal plasma contains an activator of plasminogen which was chromatographically purified. The molecular weight was determined to be 67,000.This study was supported by grants from the Swedish Medical Research Council (No. B75-17X-4523-01).     

Cultivation of arterial endothelial cells from human umbilical cord

We have developed a simple method for the isolation of endothelial cells from human umbilical artery. The method provides a sufficient number of cells to be of experimental value. The presence of factor VIII antigen specific for endothelium has been demonstrated by immunofluorescence as well as by the peroxidase-antiperoxidase immune complex method.     

Role of calcium in the histamine release induced by D-galactosamine from rat mast cells

Rat peritoneal mast cells were isolated and purified by differential centrifugation in Ficoll. Cells pooled from three to four rats were suspended at approximately 10(6) cells/ml in a buffered salt solution and incubated for 1 h at 37 degrees C in 300 microliter volumes in the absence or presence (9 X 10(-4) M) of calcium chloride. Addition of D-galactosamine hydrochloride (DGM; 2.8 X 10(-4)M) caused (in addition to basal release) a mean +/- SEM percent histamine release of 15.7 +/- 5.2 in the presence of Ca++ and 19 +/- 4.9 in the absence of Ca++ (p greater than 0.05). It is suggested that D-galactosamine does not require extracellular Ca++ for the release of histamine from the rat mast cell.