Inhibitory effects of neuropeptide Y on sympathetic neurotransmission in the rabbit iris-ciliary body

Neuropeptide Y (NPY, 1–300 nM) mediated a concentration-dependent inhibition of field stimulation-evoked ³H]norepinephrine (NE) overflow from the isolated, superfused rabbit iris-ciliary body. At equimolar concentrations (100 nM), the homologous neuropeptide peptide YY (PYY) mimicked the effects of NPY, whereas pancreatic polypeptide (PP) and the C-terminal fragment of NPY_16–36 did not modify ³H]NE release. NPY-induced inhibition of ³H]NE release was unaffected by pretreatment of tissues with atropine (100 nM) plus yohimbine (100 nM) and was nonadditive with the maximal prejunctional effects of carbamycholine or clonidine, indicating that NPY acts independently of prejunctional muscarinic or alpha₂-adrenergic receptor activity to reduce ³H]NE overflow. It is concluded that NPY is a specific, potent modulator of adrenergic neurosecretion in the rabbit iris-ciliary body. These findings confirm the role of NPY as a co-transmitter at ocular sympathetic neuroeffector junctions, either mimicking or augmenting the actions of endogenously released norepinephrine.To whom to address reprint requests.