Bradykinin B2-receptor-mediated Stimulation of Exocytotic Noradrenaline Release from Cardiac Sympathetic Neurons

1997 ◽  
Vol 29 (9) ◽  
pp. 2561-2569 ◽  
Author(s):  
Thomas Kurz ◽  
Ralph Tölg ◽  
Gert Richardt
Keyword(s):  
Noradrenaline Release ◽  
Sympathetic Neurons ◽  
Bradykinin B2 Receptor ◽  
Stimulation Of

VSM growth is stimulated in sympathetic neuron/VSM cocultures: role of TGF-β2 and endothelin

2000 ◽  
Vol 278 (2) ◽  
pp. H404-H411 ◽  
Author(s):  
Deborah H. Damon
Keyword(s):  
Transforming Growth Factor ◽  
Sympathetic Neurons ◽  
Sympathetic Nerves ◽  
Sympathetic Neuron ◽  
Vessel Growth ◽  
Coculture Model ◽  
Transforming Growth Factor Β2 ◽  
Cervical Ganglia ◽  
Stimulation Of

Sympathetic nerves are purported to stimulate blood vessel growth. The mechanism(s) underlying this stimulation has not been determined. With use of an in vitro coculture model, the present study tests the hypothesis that sympathetic neurons stimulate the growth of vascular smooth muscle (VSM) and evaluates potential mechanisms mediating this stimulation. Sympathetic neurons isolated from superior cervical ganglia (SCG) stimulated the growth of VSM. Growth of VSM in the presence of SCG (856 ± 81%) was significantly greater than that in the absence of SCG (626 ± 66%, P < 0.05). SCG did not stimulate VSM growth in transwell cocultures. An antibody that neutralized the activity of transforming growth factor-β2 (TGF-β2) inhibited SCG stimulation of VSM growth in coculture. SCG stimulation of VSM growth was also inhibited by an endothelin A receptor antagonist. These data suggest novel mechanisms for sympathetic modulation of vascular growth that may play a role in the physiological and/or pathological growth of the vasculature.

α2-Adrenoceptor-Mediated Inhibition of Electrically Evoked [3H]Noradrenaline Release from Chick Sympathetic Neurons: Role of Cyclic AMP

2002 ◽  
Vol 63 (1) ◽  
pp. 146-154 ◽  
Author(s):  
Stefan Boehm ◽  
Sigismund Huck ◽  
Gabriele Koth ◽  
Helmut Drobny ◽  
Ernst Agneter ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Noradrenaline Release ◽  
Sympathetic Neurons ◽  
Α2 Adrenoceptor

Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat

1997 ◽  
Vol 272 (5) ◽  
pp. H2369-H2376 ◽  
Author(s):  
R. L. Davisson ◽  
O. S. Possas ◽  
S. P. Murphy ◽  
S. J. Lewis
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Sympathetic Neurons ◽  
Specific Inhibitor ◽  
No Synthase ◽  
Systemic Administration ◽  
Sympathetic Chain ◽  
Low Intensity ◽  
Stimulation Of

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.

Effects of Buthus martensii Karsch scorpion venom on the release of noradrenaline from in vitro and in vivo rat preparations

1994 ◽  
Vol 72 (8) ◽  
pp. 855-861 ◽  
Author(s):  
Sylvain Foucart ◽  
Rui Wang ◽  
Pierre Moreau ◽  
Rémi Sauvé ◽  
Jacques de Champlain ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Noradrenaline Release ◽  
Sympathetic Neurons ◽  
Scorpion Venom ◽  
Dependent Manner ◽  
Release Of Noradrenaline ◽  
Adult Rat ◽  
Isolated Atria

The aim of this study was to test the neuronal effects of the Chinese Buthus martensii Karsch (BMK) scorpion venom in vivo and in vitro in order to understand the mechanism involved in the cardiovascular pressor effect of this venom. In conscious unrestrained rats, administration of 100 μg/kg i.v. BMK venom induced an increase in blood pressure, which was associated with a significant increase in plasma noradrenaline. In isolated atria, BMK also induced an increase in the stimulation-induced release of [3H]noradrenaline in a dose-dependent manner. The modulatory effect of agents acting at sympathetic prejunctional adrenoceptors on [3H]noradrenaline release was not altered by BMK venom administration. Finally, it was observed that 100 μg/mL BMK venom increased the intracellular calcium concentration in acutely dissociated sympathetic neurons from adult rat superior cervical ganglion. This action appeared to be mainly due to an influx of extracellular calcium. BMK venom induced a small rise in intracellular calcium in the absence of external calcium, indicating that it may also mobilize calcium from intracellular stores. The results observed in this study suggest that BMK venom may induce pressor responses by releasing noradrenaline from the sympathetic nerve terminals and that activation of neuronal calcium channels may be involved in that process.Key words: scorpion venom, noradrenaline release, presynaptic modulation, intracellular calcium.

Modulation of electrically evoked [3H]-noradrenaline release from cultured chick sympathetic neurons

1994 ◽  
Vol 350 (3) ◽  
Author(s):  
Clemens Allgaier ◽  
Angelika Schobert ◽  
Manuela Belledin ◽  
Rolf Jackisch ◽  
Georg Hertting
Keyword(s):  
Noradrenaline Release ◽  
Sympathetic Neurons
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