The interference of muscarinic receptors with the noradrenaline release from sympathetic nerve endings caused by nicotinic agents

1968 ◽  
Vol 259 (2) ◽  
pp. 181-182
Author(s):  
R. Lindmar ◽  
K. L�ffelholz ◽  
E. Muscholl
Keyword(s):  
Muscarinic Receptors ◽  
Noradrenaline Release ◽  
Sympathetic Nerve ◽  
Nerve Endings

scholarly journals Ang II Enhances Noradrenaline Release from Sympathetic Nerve Endings Thus Contributing to the Up-Regulation of Metalloprotease-2 in Aortic Dissection Patients' Aorta Wall

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76922 ◽  
Author(s):  
Zhipeng Hu ◽  
Zhiwei Wang ◽  
Hongbing Wu ◽  
Zhimin Yang ◽  
Wanli Jiang ◽  
...  
Keyword(s):  
Aortic Dissection ◽  
Noradrenaline Release ◽  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Ang Ii ◽  
Aorta Wall

Effects of Ketamine on In Vivo Cardiac Sympathetic Nerve Endings

2001 ◽  
Vol 38 ◽  
pp. S39-S42 ◽  
Author(s):  
Hirotoshi Kitagawa ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Hidezo Mori ◽  
Kenji Sunagawa
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve

Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF

2002 ◽  
Vol 283 (5) ◽  
pp. H1863-H1872 ◽  
Author(s):  
Chang-Seng Liang ◽  
Yoshihiro Himura ◽  
Michihiro Kashiki ◽  
Suzanne Y. Stevens
Keyword(s):  
Sympathetic Nerve ◽  
Glyoxylic Acid ◽  
Nerve Endings ◽  
Immunocytochemical Staining ◽  
Receptor Density ◽  
Cardiac Sympathetic Nerve ◽  
Uptake Inhibition ◽  
Uptake Activity ◽  
Β Receptor ◽  
Inotropic Responses

Right heart failure (RHF) is characterized by chamber-specific reductions of myocardial norepinephrine (NE) reuptake, β-receptor density, and profiles of cardiac sympathetic nerve ending neurotransmitters. To study the functional linkage between NE uptake and the pre- and postsynaptic changes, we administered desipramine (225 mg/day), a NE uptake inhibitor, to dogs with RHF produced by tricuspid avulsion and progressive pulmonary constriction or sham-operated dogs for 6 wk. Animals receiving no desipramine were studied as controls. We measured myocardial NE uptake activity using [3H]NE, β-receptor density by [125I]iodocyanopindolol, inotropic responses to dobutamine, and noradrenergic terminal neurotransmitter profiles by glyoxylic acid-induced histofluorescence for catecholamines, and immunocytochemical staining for tyrosine hydroxylase and neuropeptide Y. Desipramine decreased myocardial NE uptake activity and had no effect on the resting hemodynamics in both RHF and sham animals but decreased myocardial β-adrenoceptor density and β-adrenergic inotropic responses in both ventricles of the RHF animals. However, desipramine treatment prevented the reduction of sympathetic neurotransmitter profiles in the failing heart. Our results indicate that NE uptake inhibition facilitates the reduction of myocardial β-adrenoceptor density and β-adrenergic subsensitivity in RHF, probably by increasing interstitial NE concentrations, but protects the cardiac noradrenergic nerve endings from damage, probably via blockade of NE-derived neurotoxic metabolites into the nerve endings.

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