BASAL NITRIC-OXIDE PRODUCTION IN REGULATION OF COCHLEAR BLOOD-FLOW

Nitric oxide (NO), recently identified as endothelium-derived relaxing factor, has been shown to influence both vascular and neural function . In blood vessels, NO is produced by endothelial and smooth muscle ce lls and may play a role in regulation of cochlear blood flow. In the c entral nervous system, NO functions as a neurotransmitter involved in long term potentiation. The principle hypothesis tested in this study was that basal NO production in the cochlear blood vessels contributes to regulation of CBF. Since NO is a vasodilator, diminished NO synthe sis may decrease the level of CBF. Application of a competitive inhibi tor of NO synthase either intravenously or to the round window membran e caused a reduction in CBF. The application to the round window membr ane did not affect compound action potential thresholds. With intraven ous adminstration, the effect on CBF was dose-related and could be rev ersed with the physiologic substrate, L-arginine. These data indicate that NO is produced in the cochlear blood vessels and contributes to t he regulation of CBF.