Galanin-neuropeptide Y (NPY) interactions in central cardiovascular control:: involvement of the NPYY1 receptor subtype

The interactions between neuropeptide Y (NPY), specifically through NPY Y-1 and Y-2 receptor subtypes, and galanin [GAL(1-29)] have been analysed at the cardiovascular level. The cardiovascular effects of intracisternal coinjections of GAL(1-29) with NPY or NPY Y-1 or Y-2 agonists, as well as quantitative receptor autoradiography of the binding characteristics of NPY Y-1 and Y-2 receptor subtypes in the nucleus of the solitary tract (NTS), in the presence or absence of GAL(1-29), have been investigated. The effects of coinjections of GAL(1-29) and the NPY Y-1 agonist on the expression of c-FOS immunoreactivity in the NTS were also studied. The coinjection of NPY with GAL(1-29) induced a significant vasopressor and tachycardic action with a maximum 40% increase (P < 0.001). The coinjection of the NPY Y-1 agonist and GAL(1-29) induced a similar increase in mean arterial pressure and heart rate as did NPY plus GAL(1-29), actions that were not observed with the NPY Y-2 agonist plus GAL (1-29).GAL (1-29), 3 nm, significantly and substantially (by similar to 40%) decreased NPY Y-1 agonist binding in the NTS. This effect was significantly blocked (P < 0.01) in the presence of the specific galanin antagonist M35. The NPY Y-2 agonist binding was not modified in the presence of GAL(1-29). At the c-FOS level, the coinjection of NPY Y-1 and GAL(1-29) significantly reduced the c-FOS-immunoreactive response induced by either of the two peptides. The present findings suggest the existence of a modulatory antagonistic effect of GAL(1-29) mediated via galanin receptors on the NPY Y-1 receptor subtype and its signalling within the NTS.