Neuropeptide Y induced attenuation of catecholamine synthesis in the rat mesenteric arterial bed.

The effect of neuropeptide Y (NPY) on the basal and nerve stimulation-induced increase in norepinephrine synthesis was studied in the isolated and perfused mesenteric arterial bed of the rat. Tyrosine hydroxylation, the rate-limiting step in catecholamine (CA) biosynthesis, was assessed by measuring the accumulation of DOPA in the perfusate/superfusate overflow after perfusion of the mesenteric arterial bed with the decarboxylase inhibitor m-hydroxybenzyl hydralazine (NSD-1015). Treatment with NDS-1015 resulted in a time-dependent increase in DOPA production and nerve stimulation (8 Hz, supramaximal voltage, 2 ms duration) increased DOPA production even further.

Influence of cold stress on neuropeptide Y and sympathetic neurotransmission.

Chronic cold stress of rats (4 degrees C; 1-3 weeks) induced a marked increase in gene expression (adrenal medulla; superior cervical ganglia), tissue content (mesenteric arterial bed) and nerve stimulation-induced overflow of NPY-immunoreactivity (NPYir) from the perfused mesenteric arterial bed. In contrast increased NPY neurotransmission was offset by an apparent decrease in the evoked overflow of norepinephrine (NE) due to a presumed deactivation of NE by nitric oxide (NO), despite increased sympathetic nerve activity. The net effect of these offsetting system was no change in basal or the evoked increase in perfusion pressure (sympathetic tone).