The effect of (�)-dobutamine on adrenergic nerve endings

2004 ◽  
Vol 339-339 (1-2) ◽  
pp. 79-84 ◽  
Author(s):  
P. Fischer ◽  
A. Burger ◽  
K. H. Graefe ◽  
U. Trendelenburg
Keyword(s):  
Nerve Endings ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Endings

Interactions Between Neural and Endothelial Mechanisms in Control of Vascular Tone

Physiology ◽  
1991 ◽  
Vol 6 (2) ◽  
pp. 60-63
Author(s):  
VM Miller
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Tone ◽  
Nerve Endings ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Endings

Tone of the vascular smooth muscle is modulated by factors released from adrenergic nerve endings and the endothelium. These factors have the potential to modulate their release from each of the controlling systems.

Effects of estradiol on release and disposition of norepinephrine from nerve endings

1980 ◽  
Vol 239 (4) ◽  
pp. H450-H450 ◽  
Author(s):  
Martha A. Hamlet ◽  
Duane K. Rorie ◽  
Gertrude M. Tyce
Keyword(s):  
Electrical Stimulation ◽  
Column Chromatography ◽  
Liquid Scintillation ◽  
Direct Action ◽  
Nerve Endings ◽  
Extraneuronal Uptake ◽  
Adrenergic Nerve ◽  
Liquid Scintillation Spectrometry ◽  
Saphenous Veins ◽  
Adrenergic Nerve Endings

Studies were performed to determine whether estradiol (E2) has a direct action on the release and disposition of norepinephrine (NE) from adrenergic nerve endings in isolated superfused canine saphenous veins. [3H]NE and is labeled metabolites were separated by column chromatography with measurement by liquid scintillation spectrometry. An increase in the spontaneous overflow of total 3H, [3H]NE, and [3H]dihydroxyphenylglycol ([3H]DOPEG) that occurred with 1 and 10 microgram/ml E2 in the superfusing medium suggested that E2 either induced NE release or interfered with intraneuronal NE storage. During electrical stimulation (ES), release of [3H]NE and [3H]DOPEG exceeded controls with 1 and 10 microgram/ml E2 in the superfusate, yet total 3H was little changed. The evoked release of [3H]DOPEG showed less of an elevation over its spontaneous efflux in E2-treated veins than in nontreated veins, suggesting that E2 may block neuronal reuptake of released NE. The efflux of O-methylated deaminated metabolites during and after ES was decreased by E2 treatment, suggesting also an inhibition of extraneuronal uptake of NE.

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