Interactions between Neuropeptide Y and Noradrenaline Receptor Mechanisms in Sympathetic Vascular Control

Abstract

The presence of avian pancreatic polypeptide (APP)-like immunoreactivity (-IR) together with cate-cholamines in sympathetic cardiovascular nerves and adrenal medulla /l,2/ initiated the search for a novel endogenous peptide. After the isolation of neuropeptide Y (NPY), which has marked structural homology to APP (19 out of 36 amino acids in identical positions) /3/, it was demonstrated that NPY represented the APP-IR initially observed in cardiovascular nerves /4,5/. NPY was found both to exert potent vasoconstrictor activity /4,6/ and to depress the field stimulation-evoked twitch contractions of the vas deferens, suggesting prejunctional inhibition of noradrenaline (NA) release 74,7,0/. Furthermore, electrical stimulation of sympathetic nerves leads to release of not only NA but also of NPY-like immunoreactivity (-LI) /9,10/. Since a considerable part of the vasoconstrictor response to nerve stimulation remained after adrenoceptor blockade /6,9,10/ or NA depletion using reserpine treatment /10/, it has been suggested that NPY could represent a novel transmitter in sympathetic vascular control /see 11/. In this paper we will summarize some recent data which support that NPY fulfils several neurotransmitter criteria and is of importance in peripheral sympathetic vascular control. Furthermore, many drugs used for studies or treatment of hypertension also influence NPY mechanisms in various ways.