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.

scholarly journals Xiao-Qing-Long-Tang Maintains Cardiac Function during Heart Failure with Reduced Ejection Fraction in Salt-Sensitive Rats by Regulating the Imbalance of Cardiac Sympathetic Innervation

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Zhaoyu Li ◽  
Yongcheng Wang ◽  
Yuehua Jiang ◽  
Dufang Ma ◽  
Ping Jiang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Sympathetic Nerve ◽  
Morphological Changes ◽  
Sympathetic Innervation ◽  
Nerve Endings ◽  
Cardiac Sympathetic Innervation ◽  
Reduced Ejection Fraction

Objective. The anatomical and functional imbalances of sympathetic nerves are associated with cardiovascular disease progression. Xiao-Qing-Long-Tang (XQLT), an ancient Chinese herbal formula, has been used to treat cardiovascular diseases in eastern Asia for thousands of years. We determined the effect of XQLT in maintaining cardiac function during heart failure with reduced ejection fraction (HFrEF) with respect to its neurobiological effects in salt-sensitive rats. Methods. Dahl salt-sensitive (DS) rats were fed a high-salt diet to establish an HFrEF model and were divided into model (DS, administered normal saline) and XQL groups (administrated XQLT) randomly, with SS-13BN rats being used as the control. The bodyweight and blood pressure of rats were observed regularly. Electrocardiogram, echocardiography, and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) were determined to assess cardiac function. The sympathetic tune and myocardial morphological changes were evaluated. Western blot and qRT-PCR were used to assay the expression of the nerve growth factor (NGF) and leukemia inhibitory factor (LIF). Tyrosine hydroxylase (TH), choline acetyltransferase (CHAT), and growth-associated protein 43 (GAP43) were assayed to confirm sympathetic remodeling. The micromorphological changes in cardiac sympathetic nerve endings were observed by transmission electron microscopy. Results. Four weeks after XQLT treatment, cardiac function and bodyweight were higher and blood pressure was lower than that of the DS group. Myocardial noradrenaline (NA) increased, while the plasma NA level decreased significantly. The morphology demonstrated that XQLT significantly alleviated myocardial damage. XQLT decreased the expression of LIF, increased the expression of NGF, enhanced the TH+/GAP43+ and TH+/CHAT + positive nerve fiber density, and improved the TH and GAP43 protein expression, but had no effect on CHAT. Moreover, XQLT improved the micromorphology of sympathetic nerve endings in the myocardium. Conclusion. XQLT maintains cardiac function during HFrEF in salt-sensitive rats, in part, by regulating the imbalance of cardiac sympathetic innervation.

Elevation of either axoplasmic norepinephrine or sodium level induced release of norepinephrine from cardiac sympathetic nerve terminals

1996 ◽  
Vol 737 (1-2) ◽  
pp. 343-346 ◽  
Author(s):  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Hirotoshi Kitagawa ◽  
Yuji Takauchi ◽  
Toru Kawada
Keyword(s):  
Sympathetic Nerve ◽  
Sodium Level ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve

A new, concise dialysis approach to assessment of cardiac sympathetic nerve terminal abnormalities

1997 ◽  
Vol 272 (3) ◽  
pp. H1182-H1187 ◽  
Author(s):  
T. Yamazaki ◽  
T. Akiyama ◽  
H. Kitagawa ◽  
Y. Takauchi ◽  
T. Kawada ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Storage Capacity ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Local Administration ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Terminal ◽  
And Storage

We applied a dialysis technique to the hearts of anesthetized cats and examined whether the concentration of dialysate norepinephrine (NE) reflected NE disposition at the cardiac sympathetic nerve terminals. Dialysis probes were implanted in the left ventricular wall, and dialysate NE concentrations were measured as an index of myocardial interstitial NE levels. Stimulation of stellate ganglia significantly increased dialysate NE responses that were suppressed by local administration of an NE-releasing inhibitor (omega-conotoxin GVIA, 10 microM). Increments in basal dialysate NE levels were correlated with concentrations of a locally administered neuronal uptake blocker (desipramine; 1, 10, and 100 microM). Desipramine (100 microM) augmented stimulation-induced dialysate NE responses. Local administration of a neuronal vesicle uptake blocker (reserpine, 1 and 10 microM) did not alter dialysate NE levels but increased dialysate dihydroxyphenylglycol levels. An NE-releasing amine (tyramine, 100 microg/ml) was locally administered to examine NE storage capacity at the nerve terminal. The tyramine-induced NE-releasing response was completely abolished by pretreatment with reserpine (1 mg/kg i.p.). Thus cardiac dialysis with local administration of a pharmacological tool offers a new, concise approach to assessment of neuronal NE release, uptake, vesicle uptake, and storage capacity by cardiac sympathetic nerve terminals.

scholarly journals Sympathetic control of heart rate in nNOS knockout mice

2008 ◽  
Vol 294 (1) ◽  
pp. H354-H361 ◽  
Author(s):  
J. K. Choate ◽  
S. M. Murphy ◽  
R. Feldman ◽  
C. R. Anderson
Keyword(s):  
Heart Rate ◽  
Adenylate Cyclase ◽  
Sympathetic Nerve ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Nerve Fibers ◽  
Chronotropic Response ◽  
Isolated Atria ◽  
Sympathetic Nerve Activation ◽  
Oxide Synthase

Inhibition of neuronal nitric oxide synthase (nNOS) in cardiac postganglionic sympathetic neurons leads to enhanced cardiac sympathetic responsiveness in normal animals, as well as in animal models of cardiovascular diseases. We used isolated atria from mice with selective genetic disruption of nNOS (nNOS−/−) and their wild-type littermates (WT) to investigate whether sympathetic heart rate (HR) responses were dependent on nNOS. Immunohistochemistry was initially used to determine the presence of nNOS in sympathetic [tyrosine hydroxylase (TH) immunoreactive] nerve terminals in the mouse sinoatrial node (SAN). After this, the effects of postganglionic sympathetic nerve stimulation (1–10 Hz) and bath-applied norepinephrine (NE; 10−8–10−4 mol/l) on HR were examined in atria from nNOS−/− and WT mice. In the SAN region of WT mice, TH and nNOS immunoreactivity was virtually never colocalized in nerve fibers. nNOS−/− atria showed significantly reduced HR responses to sympathetic nerve activation and NE ( P < 0.05). Similarly, the positive chronotropic response to the adenylate cyclase activator forskolin (10−7–10−5 mol/l) was attenuated in nNOS−/− atria ( P < 0.05). Constitutive NOS inhibition with l-nitroarginine (0.1 mmol/l) did not affect the sympathetic HR responses in nNOS−/− and WT atria. The paucity of nNOS in the sympathetic innervation of the mouse SAN, in addition to the attenuated HR responses to neuronal and applied NE, indicates that presynaptic sympathetic neuronal NO does not modulate neuronal NE release and SAN pacemaking in this species. It appears that genetic deletion of nNOS results in the inhibition of adrenergic-adenylate cyclase signaling within SAN myocytes.

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.

Chemical sympathetic denervation, suppression of myocardial transient outward potassium current, and ventricular fibrillation in the rat

2008 ◽  
Vol 86 (10) ◽  
pp. 700-709 ◽  
Author(s):  
Juan Bai ◽  
Chongyu Ren ◽  
Wei Hao ◽  
Rui Wang ◽  
Ji-Min Cao
Keyword(s):  
Ventricular Fibrillation ◽  
Sympathetic Nerve ◽  
Sympathetic Innervation ◽  
Outward Current ◽  
Sympathetic Denervation ◽  
Transient Outward Current ◽  
Chemical Sympathectomy ◽  
Cardiac Sympathetic Nerve ◽  
Patch Clamp Technique ◽  
Kv Channel

Sympathetic denervation is frequently observed in heart disease. To investigate the linkage of sympathetic denervation and cardiac arrhythmia, we developed a rat model of chemical sympathectomy by subcutaneous injections of 6-hydroxydopamine (6-OHDA). Cardiac sympathetic innervation was visualized by means of a glyoxylic catecholaminergic histofluorescence method. Transient outward current (Ito) of ventricular myocytes was recorded with the whole-cell configuration of the patch clamp technique. We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of Ito channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing. Three weeks after 6-OHDA injections, which allowed time for sympathetic regeneration, we found cardiac sympathetic nerve density, norepinephrine levels, expression levels of Kv4.2 and KChIP2 proteins, and Ito densities were partially normalized and ventricular fibrillation severity was decreased. We conclude that chemical sympathectomy downregulates the expression of selective Kv channel subunits and decreases myocardial Ito channel activities, contributing to the elevated susceptibility to ventricular fibrillation.

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