Sp. Han et al., DIRECT EVIDENCE FOR THE ROLE OF NEUROPEPTIDE-Y IN SYMPATHETIC-NERVE STIMULATION-INDUCED VASOCONSTRICTION, American journal of physiology. Heart and circulatory physiology, 43(1), 1998, pp. 290-294
Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter
with norepinephrine (NE) in sympathetic nerve terminals and is thought
to be involved in sympathetic nerve stimulation (SNS)-induced vasocon
striction. Using BIBP-3226, a Y-1 receptor selective antagonist, we ex
amined this hypothesis in the isolated and perfused mesenteric vascula
r bed. SNS produced a frequency-dependent increase in perfusion pressu
re and concomitant overflow of NPY immunoreactivity in the perfusate.
[Leu(31), Pro(34)]Npy potentiated NE-induced and ATP-induced vasoconst
riction, indicating the presence and biological action of Y-1 receptor
s in this vascular bed. The potentiation effect of [Leu(31),Pro(34)]Np
y of the increase in perfusion pressure by NE, ATP, or SNS was prevent
ed by BIBP-3226. In addition, SNS-induced vasoconstriction at both hig
h and low frequencies was significantly attenuated by BIBP-3226 at a c
oncentration that completely blocked the [Leu(31),Pro(34)]Npy- induced
potentiation of the NE- or ATP-induced vasoconstrictor effect. These
results suggest that similar to 30% of vasoconstriction produced by SN
S depends on NPY in the mesenteric vascular bed.