reported that the relaxation of isolated rabbit aorta and other arteries induced by acetylcholine and other agonists for muscarinic receptors was dependent on the presence of endothelial cells within the preparations [2]. After removal of these cells, acetylcholine could no longer induce relaxation. Endothelium-dependent relaxation by acetylcholine results from the release of a diffusable relaxing substance, which was later termed endothelium-dependent relaxing factor (EDRF) [3,4]. It has been shown that this EDRF is nitric oxide (NO) [5][6][7]. Moreover, NO is involved in numerous physiological functions [8][9][10][11][12][13][14][15][16][17][18][19][20]. It inhibits platelet aggregation and adhesion and leukocyte adhesion, and modulates smooth muscle cell proliferation [8]. In the peripheral nervous system, NO is a mediator released by a widespread network of nerves [9][10][11]. It contributes to cytotoxicity against tumor cells, bacteria, viruses and microorganisms in activated macrophages [12][13][14]. In the brain, it has been shown that NO plays a physiological role in synaptic transmission by elevating the cyclic GMP (cGMP)