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When this neurological deficit is compounded by endothelial dysfunctionwhere the blood vessels themselves are stiff, inflamed, and unable to properly regulate nitric oxidethe result is catastrophic for hemodynamics

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By inhibiting dihydrofolate reductase, MTX also prevents the reduction of dihydrobiopterin (BH2) to tetrahydrobiopterin (BH4), leading to nitric oxide synthase uncoupling and increased sensitivity of T cells to apoptosis [24, 25] Other postulated mechanisms by which MTX suppresses inflammation include enhanced adenosine release [26], inhibition of trans-methylation reactions required for cellular functions, diminished accumulation of polyamines [27]