Role of nitric oxide in neurogenic vasodilation of porcine cerebral artery.

A superfusion bioassay cascade, with porcine pial arteries as donor tissues and rabbit aortic rings as detector tissues, was used to examine the role of nitric oxide (NO) in cerebral nonadrenergic, noncholinergic neurogenic vasodilation. All arteries were mechanically denuded of endothelium. In the presence of atropine (1 microM) and guanethedine (0.3 microM), transmural nerve stimulation (TNS) of cerebral arteries (CA) resulted in a frequency-dependent relaxation of phenylephrine-precontracted aortic rings. Relaxation was abolished by tetrodotoxin (2 microM) superfused onto and by cold-storage denervation of CA, suggesting that a vasodilating factor (VF) of neuronal origin in CA was released upon TNS. The VF-induced relaxation was inhibited by NW-nitro-L-arginine (0.3 mM) superfused onto CA. This inhibition was reversed by L-arginine (0.3 mM) but not D-arginine (0.3 mM). Exogenously applied NO onto CA also induced dilations of aortic rings in a concentration-dependent manner. The VF- and NO-induced dilations, which were abolished by hemoglobin (0.3 microM), and enhanced by superoxide dismutase (30 U/ml), declined to the same extent with similar time courses from the first to the second aortic ring. These findings indicate that VF and NO possess a similar labile nature and half-life, suggesting that VF is NO or a related substance. Identical frequency-response curves of TNS (2-16 Hz) and concentration-response curves of NO (10-1000 nM) further suggest that < 1000 nM of NO was released from CA upon TNS at the maximal frequency used.(ABSTRACT TRUNCATED AT 250 WORDS)