Neuropeptide Y is a vasoconstrictor and adrenergic modulator in the hamster microcirculation by acting on neuropeptide Y-1 and Y-2 receptors

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dc.contributor.authorBoric, MP
dc.contributor.authorMartinez, A
dc.contributor.authorDonoso, MV
dc.contributor.authorHuidobroToro, JP
dc.date.accessioned2025-01-21T01:34:18Z
dc.date.available2025-01-21T01:34:18Z
dc.date.issued1995
dc.description.abstractThe microvascular effects of neuropeptide Y, and two analogs with preferential affinity for different neuropeptide Y receptor subtypes, were assessed by intravital microscopy on the hamster cheek pouch. The interaction of neuropeptide Y and its analogs with noradrenaline was also studied. Superfusion with 0.1-300 nM neuropeptide Y caused a concentration-dependent reduction in microvascular conductance that was paralleled by reductions in arteriolar and venular diameters. These effects of neuropeptide Y were equipotent with noradrenaline, but slower to develop and longer-lasting than that of noradrenaline. Neuropeptide Y did not affect permeability to macromolecules, as measured by extravasation of fluorescent dextran. The neuropeptide Y Y-1 receptor agonist, [Leu(31),Pro(34)]neuropeptide Y, mimicked neuropeptide Y with similar potency but shorter duration, while neuropeptide Y-(13-36), a neuropeptide Y Y-2 receptor agonist, was at least 10-fold less potent than neuropeptide Y to induce a delayed and prolonged reduction in microvascular conductance. The joint superfusion of 1 nM neuropeptide Y plus 0.1 mu M noradrenaline did not cause synergism, nor even summation of effects, but reduced the contractile effect of noradrenaline. No synergism was observed after a 10 min priming with 1 nM neuropeptide Y, followed by its joint application with 0.1 mu M noradrenaline, but a significant vasodilation and hyperemia ensued upon stopping noradrenaline application. Priming with 1 nM [Leu(31),Pro(34)]neuropeptide Y prolonged noradrenaline vasoconstriction without evidence of hyperemia. In contrast, priming with 1 nM neuropeptide Y-(13-36) significantly antagonized noradrenaline vasoconstriction. These findings indicate that both neuropeptide Y receptor subtypes are present in arterioles and venules of the hamster, and suggest that their activation with neuropeptide Y induces a rapid (Y-1 receptor subtype activation) and a delayed (Y-2 receptor subtype activation) vasocontractile response. The interaction with noradrenaline is complex, without evidence for synergism, but neuropeptide Y Y-2 receptor activation seems to antagonize noradrenaline and/or to facilitate auto-regulatory vasodilation after the catecholamine-induced vasoconstriction.
dc.fuente.origenWOS
dc.identifier.eissn1879-0712
dc.identifier.issn0014-2999
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/97540
dc.identifier.wosidWOS:A1995TP56000004
dc.issue.numero2-3
dc.language.isoen
dc.pagina.final401
dc.pagina.inicio391
dc.revistaEuropean journal of pharmacology
dc.rightsacceso restringido
dc.subjectcheek pouch, hamster
dc.subjectmicrovascular flow
dc.subjecthyperemia
dc.subjectnoradrenaline
dc.subjectneuropeptide Y
dc.subjectneuropeptide Y Y-1 receptor
dc.subjectneuropeptide Y Y-2 receptor
dc.subject[Leu(31),Pro(34)]neuropeptide Y
dc.subjectneuropeptide Y-(13-36)
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.titleNeuropeptide Y is a vasoconstrictor and adrenergic modulator in the hamster microcirculation by acting on neuropeptide Y-1 and Y-2 receptors
dc.typeartículo
dc.volumen294
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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