Why the study?
Does L-DMA elicit inflammatory responses in rat mesenteric venules similarly to L-NAME?
Does L-DMA elicit inflammatory responses in rat mesenteric venules similarly to L-NAME?
The endogenous NO synthase inhibitor L-DMA can elicit inflammatory microvascular responses similar to synthetic inhibitors, suggesting a potential pathological role.
L-DMA elicits acute microvascular inflammation in rats similar to L-NAME; leaves open any pathological role for endogenous NOS inhibitors in humans.
The objective of this study was to determine whether an inhibitor of nitric oxide (NO) synthase (NG,NG'-dimethyl-L-arginine; L-DMA) that is produced by vascular endothelium elicits the inflammatory responses induced by synthetic analogues of L-arginine such as NG-nitro-L-arginine methyl ester (L-NAME). Leukocyte adherence and emigration, leukocyte-platelet aggregation, and albumin leakage were monitored in rat mesenteric venules exposed to different concentrations of either L-DMA or L-NAME. Increases in leukocyte adherence (7- to 9-fold) and emigration (3- to 5-fold), platelet-leukocyte aggregation, mast cell degranulation, and an enhanced albumin leakage (30-50%) were observed within 30 min after exposing the microvascular bed to either inhibitor; however, leukocyte emigration and albumin leakage responded more intensely to L-NAME than to L-DMA. The microvascular alterations and mast cell degranulation were attenuated by addition of L-arginine to the superfusate. These results suggest that the L-DMA is capable of eliciting an inflammatory response at concentrations detected in plasma under certain pathological conditions.
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Kurose et al. (1995) studied this question.
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