Chronic exposure to neuropeptide Y determines cardiac alpha 1-adrenergic responsiveness.
The onset of sympathetic innervation induces a developmental change in the cardiac alpha 1-adrenergic chronotropic response from an increase to a decrease in rate. The mechanism by which innervation induces this alteration is unknown. Neuropeptide Y (NPY), which is found abundantly in cardiac sympathetic nerve terminals, was considered as a possible mediator for this effect. Chronic conditioning by NPY in noninnervated myocyte cultures stimulated the effect of sympathetic innervation in inducing the alpha 1-inhibitory chronotropic response. Chronic conditioning by the NPY antagonist PYX-2 blocked the effect of innervation. Thus endogenous NPY may modulate alpha 1-adrenergic responsiveness during the ontogeny of cardiac sympathetic innervation.
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
L S
LS
Sun
P C
PC
Ursell
R B
RB
Robinson
D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006329:Heart Conduction System / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects*; D009478:Neuropeptide Y / Q000494:pharmacology*; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D009478:Neuropeptide Y; D011942:Receptors, Adrenergic, alpha; D010656:Phenylephrine; D014446:Tyrosine 3-Monooxygenase