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Cultured human and rat aortic smooth muscle cells were utilized in the investigation of the effect of plasmin, a fibrinolytic protease, on interleukin-1beta- (IL-1beta) induced nitric oxide metabolites generation. Results indicate that plasmin potentiates the effect of IL-1beta ina concentration-dependent manner. Plasmin used by itself cannot induced the effects observed with IL-1beta treatment.

The effect of thrombin on interleukin-1beta- (IL-1beta) mediated induction ofnitric oxide synthase activity was examined in cultured rat aortic smooth muscle cells. Results show that thrombin inhibit the release of nitrite, a nitric oxide metabolite from IL-1beta-treated vascular smooth muscle cells. Theinhibition reaction exhibited concentration dependence. Further studies reveal that thrombin inhibits the synthesis of nitric oxide-like metabolites in the IL-1beta mediated nitric oxide synthase activation.

AbstractIncreased levels of atmospheric CO2 may alter the structure and composition of plant communities by affecting how species respond to their physical and biological environment. We investigated how elevated CO2 influenced the response of paper birch ( Betula papyrifera Marsh.) and yellow birch (Betula alleghaniensis Britt.) seedlings to variation in soil moisture. Seedlings were grown for four months on a soil moisture gradient, individually and in mixed species stands, in controlled environment facilities at ambient (375 μL L–1) and elevated (700 μL L–1) atmospheric CO2. For both individually and competitively grown paper birch seedlings, there was a greater CO2 growth enhancement for seedlings watered less frequently than for well-watered seedlings. This differential change in CO2 responsiveness across the moisture gradient reduced the difference in seedling growth between high and low water levels and effectively broadened the regeneration niche of paper birch. In contrast, for yellow birch seedlings, elevated CO2 only produced a significant growth enhancement at the wet end of the soil moisture gradient, and increased the size difference between seedlings at the two ends of the gradient. Gas exchange measurements showed that paper birch seedlings were more sensitive than yellow birch seedlings to declines in soil moisture, and that elevated CO2 reduced this sensitivity. Additionally, elevated CO2 improved survival of yellow birch seedlings growing in competition with paper birch in dry stands. Thus, elevated CO2 may influence regeneration patterns of paper birch and yellow birch on sites of differing soil moisture. In the future, as atmospheric CO2 levels rise, growth of paper birch seedlings and survival of yellow birch seedlings may be enhanced on xeric sites, while yellow birch may show improved growth on mesic sites. [ABSTRACT FROM AUTHOR]

Changes in forest species composition could influence ecosystem carbon uptake rates. To understand how species differed in their contributions to canopy photosynthesis, we investigated how the dominant coniferous (eastern hemlock, Tsuga canadensis (L.) Carr.) and broad-leaved (northern red oak, Quercus rubra L.; red maple, Acer rubrum L.) species in a central Massachusetts forest differed in canopy carbon uptake rates. We considered what factors influenced in situ leaf-level photosynthesis and then used a bottom-up summation approach to estimatespecies-specific total canopy carbon uptake rates. Variation in canopy light strongly influenced leaf-level photosynthetic rates: sunlit leaves had significantly higher rates than shaded leaves, and photosynthesis increased with canopy height. Species also differed in leaf-level photosynthetic rates, with the broad-leaved species having up totwofold higher rates than hemlock. Within hemlock, needles older than 2 years had lower photosynthesis than younger needles. Variation inleaf-level photosynthesis scaled up to influence canopy carbon uptake rates. Red oak consistently had the highest canopy photosynthetic rates, while through the season, hemlock's relative contribution to carbon flux increased and that of red maple decreased. Thus, in such mixed forests, future changes in species composition could have substantial impacts on forest carbon dynamics, particularly if red oak is the primary broad-leaved species to expand at the expense of hemlock. [ABSTRACT FROM AUTHOR]

Resource competition is commonly invoked to explain negative effects of invasive plants on native plant abundance. If invasives out-compete natives, global changes that elevate resource availability may interact with invasives to exacerbate impacts on native communities. Indeed, evidence is accumulating that elevated CO(2) and N deposition decrease native biomass and simultaneously increase invasive biomass. However, superior competitive ability, and a relative increase in the magnitude of invasive impacts under elevated resource availability, remain to be definitively proven. Using model, multi-species, multi-individual riparian plant communities, where planting density was maintained by replacement of native with exotic individuals, we conducted a greenhouse, competition experiment using native (to the UK) and invaded communities exposed to ambient and elevated CO(2) (CO(2) experiment) or N availability (N experiment). We tested two hypotheses: (1) invasives are superior competitors to natives at ambient atmospheric CO(2) and N deposition; (2) negative effects of invasives on natives are exacerbated under elevated CO(2) or N availability. Our results provide some support for the first hypothesis: in the CO(2) experiment native biomass was significantly lower in invaded communities. In the N experiment, native biomass was unaffected by the presence of exotics but other characteristics (e.g. root:shoot ratios) were altered. Differences in light availability between the experiments may have modified the effects of the invasives on the native assemblages but our design did not permit us to determine this definitively. The hypothesis that elevated CO(2) and N availability benefit invasives at the expense of natives was not supported by our results. This may be explained either because the invasives showed minor responses to the resource manipulations or because native and exotic species were differentially limited by CO(2) and N. Our results confirm the expectation that invasives alter the characteristics of native assemblages but lead us to question whether elevated resource availability will magnify these effects.

Experiments were designed to determine whether the omega 3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1 beta evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1 beta in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1 beta in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L-arginine (an inhibitor of nitric oxide synthase), transforming growth factor beta 1, platelet-derived growth factorAB and thrombin. The addition of interleukin-1 beta-activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1 beta and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in vascular smooth muscle.

The present study investigated whether or not thrombin may affect the induction of nitric oxide (NO) synthase caused by interleukin-1 beta in cultured smooth muscle cells (SMCs) from the rat aorta. The release of nitrite, an oxidation product of NO, from interleukin-1 beta-activated SMCs was inhibited by thrombin. The inhibitory effect of thrombin was prevented by hirudin, a thrombin inhibitor, and required the presence of thrombin during the induction period. Under bioassay conditions, the perfusate from interleukin-1 beta-activated SMCs relaxed endothelium-denuded rat aortic rings precontracted with phenylephrine. The perfusate from untreated SMCs or cells exposed to thrombin alone or to interleukin-1 beta in combination with thrombin relaxed only minimally the detector blood vessel. These observations demonstrate that thrombin inhibits the production of NO by the inducible NO synthase in cultured vascular SMCs.