EFFECTS OF NITRO‐l‐ARGININE ON ENDOTHELIUM‐DEPENDENT RELAXATION OF CANINE CEREBRAL ARTERIES

SUMMARY 1. The effect of NG‐nitro‐l‐arginine (NO2Arg) on the relaxation of canine basilar artery was investigated and compared with those of middle cerebral and femoral arteries. 2. NO2Arg (10−7‐3 × 10−5 mol/L) inhibited the substance‐P (Sub‐P; 10−12‐10−8 mol/L) induced relaxation in the basilar artery precontracted with prostaglandin F2α (PGF2α; 10−5 mol/L) or KCl (10−2 mol/L) in a concentration‐dependent manner and a ratio of the maximum inhibition by NO2Arg (3 × 10−5 mol/L) was more than 90%. 3. The relaxation induced by A23187 (10−9‐3 × 10−6) was also abolished by NO2Arg (3 × 10−5 mol/L), but that by glyceryl trinitrate (GTN; 10−9‐3 × 10−5 mol/L) was not, in the basilar artery precontracted with PGF2α (10−5 mol/L). NG‐nitro‐d‐arginine (NO2ArgD; 3 × 10−5 mol/L) did not affect the relaxation induced by Sub‐P (10−12‐10−8 mol/L). 4. l‐arginine (l‐Arg; 3 × 10−5‐10−4 mol/L) did not inhibit Sub‐P (10−12‐10−8 mol/L) induced relaxation in the basilar artery. Pretreatment of l‐Arg (10−4 mol/L) reversed the relaxation inhibited by NO2Arg (3 × 10−6 mol/L) in the arteries. 5. NO2Arg (3 × 10−5 mol/L) inhibited the Sub‐P (10−12‐10−8 mol/L) induced relaxation in the canine middle cerebral artery as much as in the basilar artery. NO2Arg (3 × 10−5 mol/L) also inhibited Sub‐P (10−12‐10−8 mol/L) induced relaxation in the femoral artery, but the degree of the inhibition was less than that in the basilar artery. 6. These results suggest that the endothelium‐derived relaxing factor (EDRF) of canine basilar artery is mainly l‐Arg derived nitric oxide which may play a more important role in the basilar artery than the femoral artery.