Characterization of the muscarine receptor subtype on sympathetic nerve endings in the rat caudal artery

1994 ◽  
Vol 252 (2) ◽  
pp. 167-172 ◽  
Author(s):  
Albert Shen ◽  
Fred Mitchelson
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Receptor Subtype ◽  
Muscarine Receptor ◽  
Caudal Artery

scholarly journals Endothelin-1 and Norepinephrine Overflow from Cardiac Sympathetic Nerve Endings in Myocardial Ischemia

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Masashi Tawa ◽  
Satoshi Yamamoto ◽  
Mamoru Ohkita ◽  
Yasuo Matsumura
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Disease ◽  
Cardiac Dysfunction ◽  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Receptor Subtype ◽  
Clinical Settings ◽  
Cardiac Sympathetic Nerve ◽  
Detailed Understanding ◽  
Endothelin 1

In protracted myocardial ischemia, sympathetic activation with carrier-mediated excessive norepinephrine (NE) release from its nerve endings due to reversal of NE transporter in an outward direction is a prominent cause of arrhythmias and cardiac dysfunction. Endothelin-1 (ET-1) and its receptors are intimately involved in the regulation of this carrier-mediated NE overflow in protracted myocardial ischemia. The ET-1 system is often complex, sometimes involving opposing actions depending on which receptor subtype is activated, which cells are affected, and whether stimuli are endogenously generated or exogenously applied. Therefore, a detailed understanding of the ET-1 system is important for applying drugs acting on this system in clinical settings for the treatment of ischemic cardiac disease. This article provides a detailed analysis of how the ET-1 system is involved in the regulation of carrier-mediated NE release from sympathetic nerve endings in protracted myocardial ischemia.

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

scholarly journals Pharmacological characterization of a selective agonist for bombesin receptor subtype-3

2009 ◽  
Vol 387 (2) ◽  
pp. 283-288 ◽  
Author(s):  
Li Zhang ◽  
Hans-Peter Nothacker ◽  
Zhiwei Wang ◽  
Laura M. Bohn ◽  
Olivier Civelli
Keyword(s):  
Receptor Subtype ◽  
Pharmacological Characterization ◽  
Selective Agonist ◽  
Bombesin Receptor ◽  
Subtype 3

scholarly journals Identification and functional characterization of hemorphins VV-H-7 and LVV-H-7 as low-affinity agonists for the orphan bombesin receptor subtype 3

2003 ◽  
Vol 138 (8) ◽  
pp. 1431-1440 ◽  
Author(s):  
Hans-Peter Lammerich ◽  
Annette Busmann ◽  
Christian Kutzleb ◽  
Martin Wendland ◽  
Petra Seiler ◽  
...  
Keyword(s):  
Functional Characterization ◽  
Receptor Subtype ◽  
Bombesin Receptor ◽  
Subtype 3

Molecular Cloning and Pharmacological Characterization of a New Galanin Receptor Subtype

1997 ◽  
Vol 52 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Suke Wang ◽  
Tanaz Hashemi ◽  
Chaogang He ◽  
Catherine Strader ◽  
Marvin Bayne
Keyword(s):  
Molecular Cloning ◽  
Receptor Subtype ◽  
Galanin Receptor ◽  
Pharmacological Characterization

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.

Sign in / Sign up

Export Citation Format

Share Document