Mechanisms of electrical field stimulation-induced vasodilatation in the guinea-pig basilar artery: the role of endothelium.

1. The role of endothelium in neuronal vasodilatation elicited by electrical field stimulation (EFS) was investigated in preparations of the isolated guinea-pig basilar artery in which the tone was raised with prostaglandin F2 alpha. 2. In preparations with intact endothelium, EFS produced frequency-dependent dilatations which were not affected by guanethidine but were slightly yet significantly reduced by atropine (1 microM), and were blocked by tetrodotoxin (1 microM) and the nitric oxide synthase inhibitor L-NAME (10 microM). 3. Dilatations were elicited by acetylcholine (3 microM); these were blocked by L-NAME and atropine (1 microM). 4. Dilatations were elicited by nicotine (100 microM); these were blocked by L-NAME and hexamethonium (100 microM). 5. Dilation elicited by sodium nitroprusside (SNP, 3 microM) was not affected by L-NAME. 6. The inhibitory effects of L-NAME were partially prevented by L-arginine (1 microM). 7. Removal of the endothelium resulted in a significant reduction of dilatations elicited by EFS, elimination of the dilator action of acetylcholine, but enhancement of that to SNP. 8. The results suggest that EFS-induced vasodilatation is mediated in part by the nitrergic transmitter and in part endothelium derived relaxing factor (EDRF) activated by acetylcholine released from cholinergic nerves.