scholarly journals The role of adenosine A2Aand A3receptors on the differential modulation of norepinephrine and neuropeptide Y release from peripheral sympathetic nerve terminals

2006 ◽  
Vol 96 (6) ◽  
pp. 1680-1695 ◽  
Author(s):  
M. Verónica Donoso ◽  
Felipe Aedo ◽  
J. Pablo Huidobro-Toro
Keyword(s):  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Nerve Terminals ◽  
Differential Modulation ◽  
Neuropeptide Y Release

Influence of sympathetic discharge pattern on norepinephrine and neuropeptide Y release

1989 ◽  
Vol 257 (3) ◽  
pp. H866-H872 ◽  
Author(s):  
J. Pernow ◽  
J. Schwieler ◽  
T. Kahan ◽  
P. Hjemdahl ◽  
J. Oberle ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Impulse Activity ◽  
Sympathetic Nerve Stimulation ◽  
Vasoconstrictor Response ◽  
Neuropeptide Y Release ◽  
Sympathetic Discharge ◽  
Stimulation Pattern

The effects of sympathetic nerve stimulation on vasoconstrictor responses and overflow of norepinephrine (NE) and neuropeptide Y-like immunoreactivity (NPY-LI) were studied in the dog gracilis muscle and pig spleen in vivo. A continuous regular impulse activity was compared with irregular human sympathetic and regular bursting patterns. During control conditions, stimulation with the irregular activity induced larger peak vasoconstriction than the regular activity at 0.59 Hz, but not at higher frequencies in the muscle, at 0.59 and 2.0 Hz in the spleen. The nerve stimulation-evoked overflow of NE and NPY-LI from the muscle were not influenced by the pattern of stimulation. The overflow of NPY-LI, but not that of NE, from the spleen was enhanced by the irregular activity at 0.59 and 2.0 Hz, and both NPY-LI and NE overflows were enhanced by regular burst activity at 2.0 Hz. After blockade of alpha- and beta-adrenoceptors by phenoxybenzamine and propranolol, respectively, which enhanced nerve stimulation-evoked overflow of both NE and NPY-LI, the NE overflow from the muscle evoked by the irregular activity was slightly larger at 0.59 Hz but smaller at higher frequencies compared with that evoked by regular activity, whereas the detectable overflow of NPY-LI was not largely influenced by the stimulation pattern. In conclusion, both the vasoconstrictor response and the overflow of NPY-LI and NE seem to be influenced by the pattern and frequency of sympathetic nerve stimulation.

Chronic exposure to neuropeptide Y determines cardiac alpha 1-adrenergic responsiveness

1991 ◽  
Vol 261 (3) ◽  
pp. H969-H973 ◽  
Author(s):  
L. S. Sun ◽  
P. C. Ursell ◽  
R. B. Robinson
Keyword(s):  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Chronic Exposure ◽  
Developmental Change ◽  
Sympathetic Innervation ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve ◽  
Cardiac Sympathetic Innervation ◽  
Chronotropic Response ◽  
Npy Antagonist

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.

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

2015 ◽  
Vol 18 (1) ◽  
pp. 53-61 ◽  
Author(s):  
N. Ziółkowska ◽  
B. Lewczuk ◽  
B. Przybylska-Gornowicz
Keyword(s):  
Pineal Gland ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Sympathetic Nerve Fibers ◽  
Uk 14,304 ◽  
Mammalian Pineal Gland ◽  
Pharmacologically Active

Abstract Norepinephrine (NE) released from the sympathetic nerve endings is the main neurotransmitter controlling melatonin synthesis in the mammalian pineal gland. Although neuropeptide Y (NPY) co-exists with NE in the pineal sympathetic nerve fibers it also occurs in a population of non-adrenergic nerve fibers located in this gland. The role of NPY in pineal physiology is still enigmatic. The present study characterizes the effect of NPY on the depolarization-evoked 3H-NE release from the pig pineal explants. The explants of the pig pineal gland were loaded with 3H-NE in the presence of pargyline and superfused with Tyrode medium. They were exposed twice to the modified Tyrode medium containing 60 mM of K+ to evoke the 3H-NE release via depolarization. NPY, specific agonists of Y1- and Y2-receptors and pharmacologically active ligands of α2-adrenoceptors were added to the medium before and during the second depolarization. The radioactivity was measured in medium fractions collected every 2 minutes during the superfusion. NPY (0.1 – 10 μM) significantly decreased the depolarization-induced 3H-NE release. Similar effect was observed after the treatment with Y2-agonist: NPY13-36, but not with Y1-agonist: [Leu31, Pro34]-NPY. The tritium overflow was lower in the explants exposed to the 5 μM NPY and 1 μM rauwolscine than to rauwolscine only. The effects of 5 μM NPY and 0.05 μM UK 14,304 on the depolarization-evoked 3H-NE release were additive. The results show that NPY is involved in the regulation of NE release from the sympathetic terminals in the pig pineal gland, inhibiting this process via Y2-receptors.

scholarly journals Neuropeptide Y in the Adult and Fetal Human Pineal Gland

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Morten Møller ◽  
Pansiri Phansuwan-Pujito ◽  
Corin Badiu
Keyword(s):  
Pineal Gland ◽  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Mammalian Species ◽  
Nerve Fibers ◽  
Nerve Terminals ◽  
Human Fetuses ◽  
Sympathetic Nerve Fibers ◽  
Central Innervation ◽  
The Brain

Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be colocalized with noradrenaline in sympathetic nerve terminals. The peptide has been demonstrated to be present in sympathetic nerve fibers innervating the pineal gland in many mammalian species. In this investigation, we show by use of immunohistochemistry that neuropeptide Y is present in nerve fibers of the adult human pineal gland. The fibers are classical neuropeptidergic fibers endowed with largeboutons en passageand primarily located in a perifollicular position with some fibers entering the pineal parenchyma inside the follicle. The distance from the immunoreactive terminals to the pinealocytes indicates a modulatory function of neuropeptide Y for pineal physiology. Some of the immunoreactive fibers might originate from neurons located in the brain and be a part of the central innervation of the pineal gland. In a series of human fetuses, neuropeptide Y-containing nerve fibers was present and could be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is different from most rodents, where the innervation starts postnatally.

ATP-Induced Modulation of Norepinephrine Exocytosis in Human and Porcine Heart: Role of E-NTPDase1/CD39.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1869-1869 ◽  
Author(s):  
Takuji Machida ◽  
Paul M. Heerdt ◽  
Alicia C. Reid ◽  
Ulrich Schaefer ◽  
Randi B. Silver ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Sympathetic Nerve ◽  
Therapeutic Approach ◽  
Cardiac Tissue ◽  
Vascular Dysfunction ◽  
Atp Release ◽  
Nerve Terminals ◽  
Guinea Pig Heart ◽  
Novel Therapeutic

Abstract ATP co-released with norepinephrine (NE) from cardiac sympathetic nerve terminals increases NE exocytosis via a positive feedback mechanism. Since excessive NE release is an established cause of dysfunction in ischemic heart disease, we studied the role of endogenous and exogenous nucleotidases as part of the development of a novel therapeutic approach to myocardial ischemia and its consequences. Using sympathetic nerve terminals isolated from guinea pig heart (cardiac synaptosomes), we previously established that activation of ATP-gated ionotropic presynaptic P2X purinoceptors (P2XR) promotes exocytosis of NE. This effect was increased by inhibition of the endogenous ecto-nucleotidase (E-NTPDase1/CD39) and decreased by solCD39, a recombinant form of human E-NTPDasel/CD39. Furthermore, depolarization of synaptosomes with K+ also evoked NE exocytosis. This was potentiated by inhibition of E-NTPDase1 with ARL67156 (a selective E-NTPDase inhibitor), and attenuated by addition of solCD39. These findings indicated that ATP released by depolarization of sympathetic terminals enhances NE exocytosis, and that E-NTPDase1 plays an important modulatory role in adrenergic neurotransmission in the heart. In the present study, we investigated the role of E-NTPDasel in exocytosis of NE and ATP in porcine as well as human heart. Cardiac E-NTPDase1 is selectively localized in human and porcine cardiac neurons, and depolarization of cardiac tissue elicits an ω-conotoxin-inhibitable release of both NE and ATP. Inhibition of E-NTPDase1 with ARL67156 markedly potentiated release of ATP, demonstrating that E-NTPDase1 is a major control system for ATP availability at sympathetic nerve endings. Importantly, when ATP exocytosis was increased via inhibition of E-NTPDase1, NE exocytosis increased in parallel. Moreover, when ATP release was reduced by administration of solCD39, NE exocytosis was markedly diminished. Thus, ATP regulates NE exocytosis by activating presynaptic P2XR. This concept is further validated by our finding that the strong correlation between ATP and NE release was abolished by the P2XR antagonist PPADS. We conclude that released ATP governs NE exocytosis by activating presynaptic P2XR and that this is controlled by E-NTPDase1/CD39. Clinically, excessive NE release is a major cause of arrhythmic and coronary vascular dysfunction during myocardial ischemia. By curtailing NE release, solCD39 may offer a novel therapeutic approach to ischemic complications in the myocardium in addition to its role as an anti-thrombotic agent.

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