Garthwaite J, Garthwaite G, Palmer R M, Moncada S
Department of Physiology, University of Liverpool, U.K.
Eur J Pharmacol. 1989 Oct 17;172(4-5):413-6. doi: 10.1016/0922-4106(89)90023-0.
Activation of N-methyl-D-aspartate (NMDA) receptors in rat cerebellum leads to the release of endothelium-derived relaxing factor, now identified as nitric oxide (NO), a stimulator of soluble guanylate cyclase. L-NG-monomethylarginine (L-NMMA), which blocks NO synthesis from L-arginine in several tissues, including a crude synaptosomal preparation from brain, inhibited the elevation of cyclic GMP induced by NMDA in rat cerebellar slices. D-NMMA was ineffective. L-Arginine, but not its D enantiomer, augmented the response to NMDA and reversed the inhibition by L-NMMA. The results indicate that stimulation of NMDA receptors results in the activation of the enzyme which catalyzes the formation of NO from L-arginine.
大鼠小脑中N-甲基-D-天冬氨酸（NMDA）受体的激活会导致内皮源性舒张因子的释放，现在已确定该因子为一氧化氮（NO），它是可溶性鸟苷酸环化酶的刺激物。L-NG-单甲基精氨酸（L-NMMA）可阻断包括脑粗突触体在内的多种组织中由L-精氨酸合成NO，它抑制了NMDA诱导的大鼠小脑切片中环鸟苷酸（cGMP）的升高。D-NMMA则无效。L-精氨酸而非其D型对映体增强了对NMDA的反应，并逆转了L-NMMA的抑制作用。结果表明，NMDA受体的刺激会导致催化由L-精氨酸形成NO的酶的激活。
