NG-nitro-l-arginine methyl ester-induced norepinephrine release from cardiac sympathetic nerve endings in anesthetized cats

2003 ◽  
Vol 353 (3) ◽  
pp. 205-208 ◽  
Author(s):  
Yuji Takauchi ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Kenji Sunagawa
Keyword(s):  
Methyl Ester ◽  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release

EctoNucleotidase in Cardiac Sympathetic Nerve Endings Modulates ATP-Mediated Feedback of Norepinephrine Release

2002 ◽  
Vol 300 (2) ◽  
pp. 605-611 ◽  
Author(s):  
Casilde Sesti ◽  
M. Johan Broekman ◽  
Joan H. F. Drosopoulos ◽  
Naziba Islam ◽  
Aaron J. Marcus ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release

Presynaptic effects of epinephrine on norepinephrine release from cardiac sympathetic nerves in dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H205-H211 ◽  
Author(s):  
G. Boudreau ◽  
F. Peronnet ◽  
J. De Champlain ◽  
R. Nadeau
Keyword(s):  
Left Ventricle ◽  
Intravenous Administration ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Facilitatory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release ◽  
Epinephrine Infusion ◽  
Beta 2

The possible functional role of tissue epinephrine in the modulation of norepinephrine release from cardiac sympathetic nerve endings in anesthetized dog was investigated. Observations were carried out under control conditions and after a short- (10 min) and long-term (180 min) epinephrine infusion (92 ng.kg-1.min-1). An increase in the stimulation-induced release of norepinephrine after intravenous administration of a selective beta 2-agonist (fenoterol, 0.5 micrograms/kg) indicated the presence of the beta 2-facilitatory mechanism. Furthermore, the facilitatory effect of fenoterol was inhibited by intravenous administration of a selective beta 2-antagonist (ICI 118551, 1 mg/kg). Short-term epinephrine infusion did not facilitate the stimulation-induced release of norepinephrine, when tissue epinephrine content in the left ventricle was increased 1.5-fold, without, as well as with, alpha 2-blockade (yohimbine, 0.3 mg/kg). However, stimulation-induced release of norepinephrine from the myocardium was significantly potentiated in animals in which tissue epinephrine in the left ventricle was greatly increased (5.6-fold) by a prolonged infusion of epinephrine (180 min). It is concluded that a facilitatory mechanism mediated by presynaptic beta 2-adrenoceptors is present in cardiac sympathetic nerve endings of the dog. Some of our observations support the hypothesis that this mechanism may be influenced by locally released epinephrine and, thus, by tissue epinephrine content.

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.

Bradykinin B2-Receptor Activation Augments Norepinephrine Exocytosis From Cardiac Sympathetic Nerve Endings

1997 ◽  
Vol 81 (5) ◽  
pp. 774-784 ◽  
Author(s):  
Nahid Seyedi ◽  
Terrance Win ◽  
Harry M. Lander ◽  
Roberto Levi
Keyword(s):  
Sympathetic Nerve ◽  
Receptor Activation ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Bradykinin B2 Receptor

Effects of moderate hypothermia on in situ cardiac sympathetic nerve endings

2002 ◽  
Vol 40 (3) ◽  
pp. 235-242 ◽  
Author(s):  
Hirotoshi Kitagawa ◽  
Tsuyoshi Akiyama ◽  
Toji Yamazaki
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Moderate Hypothermia ◽  
Cardiac Sympathetic Nerve

scholarly journals Effect of sustained limb ischemia on norepinephrine release from skeletal muscle sympathetic nerve endings

2006 ◽  
Vol 49 (5) ◽  
pp. 448-453 ◽  
Author(s):  
Yosuke Kuroko ◽  
Noriyuki Tokunaga ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Kozo Ishino ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sympathetic Nerve ◽  
Limb Ischemia ◽  
Nerve Endings ◽  
Norepinephrine Release

Effect of Bupivacaine and Levobupivacaine on Exocytotic Norepinephrine Release from Rat Atria

2005 ◽  
Vol 102 (5) ◽  
pp. 977-984 ◽  
Author(s):  
Antony Joseph ◽  
Raul Montiague ◽  
Ali R. Effendi ◽  
Renata A. Urbanska ◽  
Stephen Vogel ◽  
...  
Keyword(s):  
Local Anesthetics ◽  
Inhibitory Concentration ◽  
Inhibitory Effect ◽  
Contractile Force ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve ◽  
Norepinephrine Release ◽  
Sympathetic Neurotransmission ◽  
Rat Atria ◽  
Sympathetic Reflexes

Background The cardiotoxic mechanism of local anesthetics may include interruption of cardiac sympathetic reflexes. The authors undertook this investigation to determine if clinically relevant concentrations of bupivacaine and levobupivacaine interfere with exocytotic norepinephrine release from cardiac sympathetic nerve endings. Methods Rat atria were prepared for measurements of twitch contractile force and [H]-norepinephrine release. After nerve endings were loaded with [H]-norepinephrine, the tissue was electrically stimulated in 5-min episodes during 10 10-min sampling periods. After each period, a sample of bath fluid was analyzed for radioactivity and [H]-norepinephrine release was expressed as a fraction of tissue counts. Atria were exposed to buffer alone during sampling periods 1 and 2 (S1 and S2). Control atria received saline (100 microl each, n = 6 atria) in S3-S10. Experimental groups (n = 6 per group) received either bupivacaine or levobupivacaine at concentrations (in microM) of 5 (S3-S4), 10 (S5-S6), 30 (S7-S8), and 100 (S9-S10). Results Bupivacaine and levobupivacaine decreased stimulation-evoked fractional [H]-norepinephrine release with inhibitory concentration 50% values of 5.1 +/- 0.5 and 6.1 +/- 1.3 microM. The inhibitory effect of both local anesthetics (approximately 70%) approached that of tetrodotoxin. Local anesthetics abolished the twitch contractions of atria with inhibitory concentration 50% values of 12.6 +/- 5.0 microM (bupivacaine) and 15.7 +/- 3.9 microM (levobupivacaine). In separate experiments, tetrodotoxin inhibited twitch contractile force by only 30%. Conclusions The results indicate that clinically relevant cardiotoxic concentrations of bupivacaine and levobupivacaine markedly depress cardiac sympathetic neurotransmission. A possible mechanism of local anesthetics in reducing evoked norepinephrine release from sympathetic endings is blockade of tetrodotoxin-sensitive fast sodium channels.

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