Stimulation of the sympathetic perimesenteric arterial nerves releases neuropeptide Y potentiating the vasomotor activity of noradrenaline: Involvement of neuropeptide Y-Y-1 receptors

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dc.contributor.authorDonoso, MV
dc.contributor.authorBrown, N
dc.contributor.authorCarrasco, C
dc.contributor.authorCortes, V
dc.contributor.authorFournier, A
dc.contributor.authorHuidobroToro, JP
dc.date.accessioned2025-01-21T01:33:09Z
dc.date.available2025-01-21T01:33:09Z
dc.date.issued1997
dc.description.abstractNeuropeptide Y (NPY) appears to be involved in the sympathetic regulation of vascular tone. To assess the putative role of NPY in mesenteric circulation, the release and biological effect of NPY were examined after electrical stimulation of perimesenteric arterial nerves, Nerve stimulation with trains of 2-30 Hz increased the perfusion pressure of the arterially perfused rat mesenteric bed in a frequency-and time-dependent fashion, Trains of 15-30 Hz significantly displaced to the left, approximately threefold, the noradrenaline (NA)-induced presser concentration-response curve, in addition to increasing significantly its efficacy. Perfusion with 10 nM exogenous NPY mimicked the electrical stimulation effect, causing a threefold leftward shift of the NA concentration-response curve and increasing the maximal NA response. These effects were antagonized by 100 nM BIBP 3226, indicating the activity of NPY-Y-1 receptors. Electrical stimulation of the perimesenteric nerves released immunoreactive NPY (ir-NPY) in a frequency-dependent fashion; the ir-NPY coelutes with synthetic NPY as confirmed by HPLC. Both the electrically induced presser response and the calcium-dependent release of NPY were obliterated in preparations perfused with 1 mu M guanethidine or in rats pretreated intravenously for 48 h with 6-hydroxydopamine, thus revealing the sympathetic origin of these phenomena. Only a small proportion of the total NPY content in the perimesenteric arterial nerves is released after electrical stimulation. Chromatographic studies of the physiological sources of the ir-NPV support that NPY fragments are generated via peptidase degradation. The present findings demonstrate that NPY is re[eased from the perimesenteric arterial sympathetic nerves and acts, via the activation of NPY-Y-1 receptors, as the mediator responsible for the potentiation of NA's effect on perfusion pressure in the isolated rat mesenteric bed.
dc.fuente.origenWOS
dc.identifier.eissn1471-4159
dc.identifier.issn0022-3042
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/97378
dc.identifier.wosidWOS:A1997XR46700018
dc.issue.numero3
dc.language.isoen
dc.pagina.final1059
dc.pagina.inicio1048
dc.revistaJournal of neurochemistry
dc.rightsacceso restringido
dc.subjectCa2+-dependent neuropeptide Y release
dc.subjectneuropeptide Y chromatographic identification
dc.subjectneuropeptide Y-induced noradrenaline potentiation
dc.subjectmesenteric nerves
dc.subjectmesenteric circulation
dc.subject.ods02 Zero Hunger
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa02 Hambre cero
dc.subject.odspa03 Salud y bienestar
dc.titleStimulation of the sympathetic perimesenteric arterial nerves releases neuropeptide Y potentiating the vasomotor activity of noradrenaline: Involvement of neuropeptide Y-Y-1 receptors
dc.typeartículo
dc.volumen69
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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