Halothane decreases the release of neuropeptide Y and 3,4-dihydroxyphenylglycol from superfused segments of dog pulmonary artery.

Neuropeptide Y (NPY), norepinephrine (NE), and 3,4-dihydroxyphenylglycol (DOPEG), the metabolite of NE that arises intraneuronally, were measured in superfusates before, during, and after nerve stimulation and in extracts of dog pulmonary artery after superfusion and electrical stimulation (ES) at 12, 6, and 1 Hz. NE and DOPEG were quantified by high-pressure liquid chromatography with electrochemical detection; peptides were quantified by radioimmunoassay. The rate of overflow of NPY, NE, and DOPEG into superfusate was measured over time. The overflow of DOPEG into superfusate during basal conditions was 3.0 times that of NE. Efflux of DOPEG and NPY increased during ES; peak effluxes were not reached, however, until after cessation of stimulation. NE efflux peaked during ES. Effluxes of NE, NPY, and DOPEG were frequency-dependent at 12 and 6 Hz; at 1 Hz efflux of only NE was greater than basal. Halothane decreased significantly the rates of NPY and DOPEG efflux during and after 12 Hz ES; DOPEG efflux evoked by 6 Hz stimulation was also decreased by halothane. The percentage of the total tissue content of NPY that overflowed was decreased by halothane. Halothane did not affect the molar ratios of NE:DOPEG or NE:NPY during basal conditions or ES. These studies provide evidence that halothane slows efflux of NPY that is released along with NE from dog pulmonary artery during high frequencies of stimulation. Halothane also reduces the metabolism of NE to DOPEG.