Chemical sympathectomy by selective destruction of adrenergic nerve endings with 6-hydroxydopamine

1968 ◽  
Vol 261 (3) ◽  
pp. 271-288 ◽  
Author(s):  
H. Thoenen ◽  
J. P. Tranzer
Keyword(s):  
Nerve Endings ◽  
Adrenergic Nerve ◽  
Chemical Sympathectomy ◽  
Selective Destruction ◽  
Adrenergic Nerve Endings ◽  
6 Hydroxydopamine

The Effect of Cocaine, Reserpine, and 6-Hydroxydopamine on the Response of the Perfused Central Artery of the Rabbit Ear to Sympathomimetic amines

1975 ◽  
Vol 53 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Man Sen Yong ◽  
Pi-Chuan Chen
Keyword(s):  
Nerve Endings ◽  
Adrenergic Nerve ◽  
Sympathomimetic Amines ◽  
Central Artery ◽  
Ear Artery ◽  
Rabbit Ear ◽  
Uptake Process ◽  
Adrenergic Nerve Endings ◽  
The Difference ◽  
6 Hydroxydopamine

The perfused central artery of the rabbit ear was less sensitive to extraluminal than to intraluminal noradrenaline, but the reverse was true for metaraminol, methoxamine, metanephrine, and isoproterenol. No difference was noted between the extraluminal and intraluminal potency of phenylephrine. Cocaine potentiated the effect of extraluminal and intraluminal noradrenaline, but decreased that of intraluminal phenylephrine. Irrespective of the route of administration, the constrictor potencies of other sympathomimetic amines were not affected by cocaine. Arteries of reserpine-treated rabbits were supersensitive to extraluminally and intraluminally applied noradrenaline and phenylephrine, but they were not supersensitive to metaraminol. 6-Hydroxydopamine effectively destroyed adrenergic nerve endings of the central ear artery and increased its responses to both extraluminal and intraluminal noradrenaline and phenylephrine. However, only the constrictor potencies of intraluminally applied metaraminol and methoxamine were enhanced by 6-hydroxydopamine. The apparent discrepancies between the results obtained by various procedures that eliminate or impair the nerve uptake process suggest that the difference in the constrictor potency of extraluminal and intraluminal sympathomimetic amines is probably unrelated to their uptake by nerves located in the adventitio–medial junction of the artery.

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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