The presence of the neuronal isoform of nitric oxide synthase (nNOS) in astrocytes and neurons as well as in the perivascular nerves and cerebrovascular endothelium is well documented. The role of the nNOS, however, is not yet understood. In the present study, the function of cerebrovascular nNOS was investigated by comparing the effects of the specific nNOS blocker 7-nitro indazole monosodium salt (7-NINA) to that of the general NOS inhibitor NG-nitro-L-arginine (L-NA) in isolated rat basilar arteries (BAs). 7-NINA had no significant effect on the resting tone of the vessels, while L-NA induced strong contraction. The relaxant effect of bradykinin was attenuated in the presence of L-NA but was not changed by 7-NINA. In contrast, 7-NINA markedly reduced the acetylcholine-induced, endothelium-dependent relaxation. These results demonstrate that nNOS contributes significantly to the relaxant effect of acetylcholine, indicating the functional importance of this isoenzyme in the cerebrovascular endothelium.
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