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The transmission of impulses from sympathetic nerve terminals to target cells is mediated by noradrenaline. The action potentials open voltage-dependent calcium channels (VDCCs) in the nerve terminals and the resulting increase of the free intraterminal concentration of calcium ([Ca2+]i) causes calcium-dependent liberation of noradrenaline. The action potential-evoked release of transmitters is subjected to modulation by the transmitter itself and by other neurotransmitters that can occur at the level of the cell bodies or at the level of the nerve terminals (9). The effect on the cell bodies usually affects the propensity of neurons to fire action potentials whereas that on the nerve terminals is often a consequence of a changes in calcium influx.

Nitric oxide (NO), which has recently been shown to subserve an extraordinary diverse range of physiological functions in vivo, was first recognised as an endothelial derived relaxing factor in blood-vessels (1, 2), and has been identified recently as an important second messenger or neurotransmitter in both the central and peripheral nervous systems (2, 3). NO is apparently formed under the catalysis of NO synthase (NOS) from L-arginine via oxidation of one of the guanidino groups of arginine with the stoichiomet- ric formation of L-citrulline (4). The NOS protein is at least three different isoforms have so far been identified, and the form present in neural and endothelial tissue is constitu- tively expressed whereas that in macrophage is inducibly expressed. Neural NOS has been identified in the central nervous system such as in the cerebellum and in the supraoptic nuclei of the hypothalamus, and in the peripheral nervous system, such as in adrenal medulla. NO is considered to play an important physiological role even in these tissues. However, few investigations have been performed on the effects of NO on catecholamine (CA) release from adrenal chromaffin cells, so that the authentic physiological significance of NO on the cells is still unknown.