EFFECTS OF ARGININOSUCCINIC ACID ON NITRIC OXIDE‐MEDIATED RELAXATIONS IN RAT AORTA AND ANOCOCCYGEUS MUSCLE

1. Argininosuccinic acid (ASA), a naturally occurring N^G derivative of arginine, and the nitric oxide synthase (NOS) inhibitor JV^G‐nitro‐L‐arginine methyl ester (l‐NAME) were compared for their ability to reduce responses to nitric oxide (NO) derived from endothelial cells (aorta) and nitrergic nerves (anococcygeus muscle). 2. In isolated rings of rat aorta, endothelium‐dependent relaxation responses to acetylcholine were abolished by l‐NAME (0.1 mmol/L) and were reduced by ASA (0.1 and 0.3 mmol/L). Relaxations induced by sodium nitroprusside (SNP) were not affected by l‐NAME but were reduced by ASA. 3. In rat isolated anococcygeus muscles, relaxations elicited by nitrergic nerve stimulation at 1 Hz were abolished by l‐NAME (0.1 mmol/L) but were only slightly reduced by ASA (1 mmol/L). The effect of ASA was not sustained. l‐Arginine (1 mmol/L) prevented the effect of L‐NAME but not that of ASA. Neither ASA or l‐NAME inhibited SNP‐induced relaxation in the anococcygeus muscle. 4. The results suggest that ASA inhibits NOS but this does not totally account for its effects in reducing NO‐mediated relaxations produced by the endothelium‐dependent vasodilator acetylcholine in rat aortic rings and stimulation of nitrergic nerves in the rat anococcygeus muscle.