The Galanin N-terminal fragment (1–15) interacts with neuropeptide Y in central cardiovascular control: Involvement of the NPY Y2 receptor subtype

The interactions between neuropeptide Y (NPY), specifically through NPY Y1 and Y2 receptor subtypes and the Galanin N-terminal fragment (1–15) [GAL(1–15)] were analyzed at the cardiovascular level. The cardiovascular effects of intracisternal coinjections of GAL(1–15) and NPY, NPY Y1 or Y2 agonist have been investigated as well as quantitative receptor autoradiography of the binding characteristics of NPY Y1 and Y2 receptor subtypes in the nucleus of the solitary tract (NTS) in the presence or absence of GAL(1–15). The coinjection of NPY with GAL(1–15) induces a significant vasopressor action. The coinjection of the NPY Y2 agonist and GAL(1–15) induced a similar increase of mean arterial pressure as induced by NPY + GAL(1–15), actions that were not observed with the NPY Y1 agonist + GAL(1–29). No interactions were observed at heart rate level. GAL(1–15) 3 nM significantly and substantially increased NPY-Y2 agonist binding in the NTS by about 50%. This effect was significantly blocked (p < 0.01) in the presence of the specific Galanin antagonist M40. The NPY-Y1 agonist binding was not modified in the presence of GAL(1–15). The present findings suggest the existence of a facilitatory effect of GAL(1–15) mediated via Galanin receptors on the NPY Y2 receptor subtype and its cardiovascular function within the NTS.