Abstract
An interesting and potentially very important study1 in this issue of Circulation Research reports that during development of the mammalian heart, neuropeptide Y can significantly increase L-type Ca2+ current, thereby enhancing heart rate and strength of contraction. In this study, a combination of targeted deletion of the NPY gene, electrophysiological recordings, and immunoblot analysis of Ca2+ channel α1C expression is used in an experimental design that involves study of hearts from pre- and postnatal animals at predetermined stages.1 These findings can perhaps be put in context by the following brief review of NPY physiology and pharmacology in mammalian tissue. Neuropeptide Y (NPY) was identified by Tatemoto and Mutt in 1982 through use of a novel chemical assay that detected the amidated C-terminal tyrosine residue of this 36-amino acid peptide.2,3 Isolated first from brain, it was soon discovered to be widely distributed throughout the body, primarily in postganglionic sympathetic nerves and often colocalized with norepinephrine.4 Indeed, NPY is the most widely distributed and abundant neuropeptide in the nervous system. NPY shares structural and functional homology with two other 36-amino acid peptides, pancreatic polypeptide (PP) and peptide YY (PYY).4 All …
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