THE NITRERGIC TRANSMITTER OF THE ANOCOCCYGEUS - NO OR NOT

Nonadrenergic noncholinergic (NANC) relaxations of the anococcygeus mu scle are reduced by inhibitors of nitric oxide synthase (NOS). Since N OS can be detected within 6-hydroxydopamine-resistant nerve tracts run ning through the muscle, it seems clear that these NANC relaxations re sult from activation of the L-arginine/NO pathway within the prejuncti onal nerve terminal, an example of so-called ''nitrergic'' transmissio n. However, a number of substances (hydroquinone, superoxide anions, h ydroxocobalamin) profoundly reduce relaxations to exogenous NO but do not affect those to nitrergic field stimulation; such observations hav e raised questions over the nature of the substance actually released from the nitrergic nerves. Several possible explanations are discussed : (1) NO is released attached to a carrier molecule, perhaps in the fo rm of a nitrosothiol; (2) NO is released in a modified redox form; (3) NO is released as a free radical, but is protected within the neuroef fector junction by other substances which preferentially interact with scavenger molecules; and (4) NO is released as a free radical and, be cause of a rapid and unhindered rate of diffusion over short distances (100-200 mu M), it is less susceptible than exogenous NO to scavenger molecules. As yet, there is insufficient experimental evidence to dec ide which, if any, of these explanations is correct.