Neuropeptide Y: Neurotransmitter or Trophic Factor in the Heart?

Abstract

Neuropeptide Y (NPY) is released from sympathetic neurons and exerts short-term (acute) effects on prejunctional nerve terminals and postjunctional cardiac ion channels. However, NPY also exerts long-term (trophic) effects on angiogenesis, cardiac hypertrophy, autonomic signaling, and cardiac ion channels, including effects on L-type Ca2+ and pacemaker channels.

Potential players in the hood

“…Using myocardial neuronal cocultures, labs have now defined some aspects of how neurons first impact the cardiac phenoptype [8][9][10]. One of us has studied intensely how sustained sympathetic innervation regulates ion channel expression and autonomic responsiveness and how some of these effects can be ascribed to NPY acting as a trophic factor [11,12].…”

Neuropeptide Y T1128C polymorphism

“…In vitro, NPY exerts both postjunctional inotropic and chronotropic effects on cardiac tissue involving L-type Ca 2+ currents and pacemaker currents by acting on specific pre-and postsynaptic receptors [1,7]. NPY also induces cardiac hypertrophy by stimulating cardiac myocyte growth, and angiogenic effects by promoting vascular sprouting and capillary tube formation by endothelial cells [7,8]. In vivo, the cardiovascular actions of NPY are more complex and appear to depend on the species and the site or mode of administration; these effects are often difficult to reconcile from one study to another [1].…”

“…However, following its discovery, NPY has been shown to exert diverse biological actions on central and peripheral neural regulation, cholesterol metabolism, appetite and behaviour, and cardiovascular and blood pressure homeostasis. The neural and cardiovascular effects of NPY and its possible role in hypertension have been the subject of several recent reviews [1,[4][5][6][7]. In vitro, NPY exerts both postjunctional inotropic and chronotropic effects on cardiac tissue involving L-type Ca 2+ currents and pacemaker currents by acting on specific pre-and postsynaptic receptors [1,7].…”

“…Information derived from these studies may be useful in devising new strategies to prevent and treat human disease. Because of its potential effects on cardiovascular and blood pressure regulation [1,4,5,7], the association between NPY gene polymorphism and cardiovascular diseases has been the focus of several studies in animals and humans. Although the study by Wallerstedt et al [9] was not the first attempt to identify an association between the NPY T1128C polymorphism and cardiovascular risks, their findings are the first to link the T1128C polymorphism to myocardial infarction and/or stroke in a hypertensive population.…”

“…The neural and cardiovascular effects of NPY and its possible role in hypertension have been the subject of several recent reviews [1,[4][5][6][7]. In vitro, NPY exerts both postjunctional inotropic and chronotropic effects on cardiac tissue involving L-type Ca 2+ currents and pacemaker currents by acting on specific pre-and postsynaptic receptors [1,7]. NPY also induces cardiac hypertrophy by stimulating cardiac myocyte growth, and angiogenic effects by promoting vascular sprouting and capillary tube formation by endothelial cells [7,8].…”