Impacts of invasive plant species on riparian plant assemblages: interactions with elevated atmospheric carbon dioxide and nitrogen deposition.

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.

Platelets inhibit the induction of nitric oxide synthesis by interleukin-1 beta in vascular smooth muscle cells.

We have investigated the role of platelets in regulating the hemostatic and vasomotor properties of vascular smooth muscle. Experiments were performed to examine the effect of the releasate from activated platelets on the production of nitric oxide from interleukin-1 beta (IL-1 beta)-treated cultured rat aortic smooth muscle cells. Treatment of vascular smooth muscle cells with IL-1 beta resulted in significant accumulation of nitrite in the culture media and in marked elevation of intracellular cyclic guanosine monophosphate (GMP) levels.

Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells.

Experiments were designed to examine whether or not insulin-like growth factor I (IGF-I), which is produced by vascular cells in response to injury, affects the production of nitric oxide evoked by the inducible nitric oxide synthase in cultures of smooth muscle cells from the rat aorta. Nitric oxide production was assessed indirectly by the measurement of nitrite accumulation and nitric oxide synthase activity by determining the formation of L-citrulline from L-arginine. Nitric oxide synthase was induced in vascular smooth muscle cells that had been exposed to interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha).

Eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells.

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.

Plasmin potentiates induction of nitric oxide synthesis by interleukin-1 beta in vascular smooth muscle cells.

Experiments were performed to examine the effect of the major fibrinolytic protease, plasmin, on the production of nitric oxide from interleukin-1 beta (IL-1 beta)-treated cultured human and rat aortic smooth muscle cells. Incubation of vascular smooth muscle cells with IL-1 beta resulted in significant accumulation of nitrite and nitrate in the culture media. Plasmin, either added exogenously or generated by the reaction of tissue plasminogen activator with plasminogen, potentiated the IL-1 beta-mediated release of nitrite and nitrate from smooth muscle cells in a concentration-dependent manner, without affecting the production of nitrite and nitrate from cells untreated with IL-1 beta.

Thrombin inhibits induction of nitric oxide synthase in vascular smooth muscle cells.

Experiments were designed to examine whether thrombin affects the production of nitric oxide-like factor(s) evoked by interleukin-1 beta (IL-1 beta) in cultured smooth muscle cells from the rat aorta. IL-1 beta stimulated the release of nitrite (a stable oxidation product of nitric oxide) from cultured smooth muscle cells. Thrombin inhibited in a concentration-dependent manner the release of nitrite caused by IL-1 beta.

The inducible nitric oxide synthase is impaired by thrombin in vascular smooth muscle cells.

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.