DMPP and the adrenergic nerve terminal: Mechanisms of noradrenaline release from vesicular and extravesicular compartments

1977 ◽  
Vol 300 (2) ◽  
pp. 131-138 ◽  
Author(s):  
H. J. Holbach ◽  
R. Lindmar ◽  
K. L�ffelholz
Keyword(s):  
Nerve Terminal ◽  
Noradrenaline Release ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminal

Role of the Adrenergic Nerve Terminal in Digitalis-Induced Cardiac Toxicity

1982 ◽  
Vol 4 (1) ◽  
pp. 91-98 ◽  
Author(s):  
Claire M. Lathers ◽  
Judy L. Gerard-Ciminera ◽  
Steven I. Baskin ◽  
John C. Krusz ◽  
Gerald J. Kelliher ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Cardiac Toxicity ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminal

Inhibitory Receptors on the Adrenergic Nerve Terminal

1979 ◽  
pp. 281-287 ◽  
Author(s):  
J.P. Long ◽  
D.B. Rusterholz ◽  
J.R. Flynn ◽  
J.G. Cannon
Keyword(s):  
Nerve Terminal ◽  
Adrenergic Nerve ◽  
Inhibitory Receptors ◽  
Adrenergic Nerve Terminal

The mechanism of [3H]noradrenaline release by histamine and its analogs from the rat vas deferens

1991 ◽  
Vol 69 (4) ◽  
pp. 469-474 ◽  
Author(s):  
N. J. Boudreau ◽  
M. M. Vohra
Keyword(s):  
Noradrenaline Release ◽  
Metabolic Profile ◽  
Vas Deferens ◽  
Neuronal Uptake ◽  
Major Constituent ◽  
Adrenergic Nerve ◽  
Qualitative And Quantitative ◽  
Ability To Act ◽  
Adrenergic Nerve Terminals ◽  
Uptake Process

In this study the mechanism by which histamine and H1 and H2 agonists evoked an overflow of radioactivity from rat vasa deferentia preloaded with [3H]noradrenaline was investigated. The overflow evoked by the various agonists was unaffected by the presence of such receptor antagonists as propranolol, phentolamine, cimetidine, or scopolamine. On the other hand, the overflow evoked by all agonists except dimaprit was inhibited by mepyramine and by two well-known neuronal uptake inhibitors, cocaine and desipramine. The inhibition by mepyramine has been attributed to its effect on the neuronal uptake process. Metabolic profile studies showed that 3,4-dihydroxyphenylglycol (DOPEG) was the major constituent in the evoked overflow caused by histamine, 2-methylhistamine, 4-methylhistamine, and dimaprit and that the overflow evoked by 2-pyridylethylamine and 2-thiazolylethylamine consisted predominantly of unchanged noradrenaline. Based on these findings, it is concluded that all of the agonists tested evoke noradrenaline release intraneuronally by entering the adrenergic nerve terminals. While dimaprit might enter by passively diffusing into the adrenergic nerves, other agonists seem to use the neuronal uptake process. Noradrenaline released intraneuronally is subsequently degraded by neuronal monoamine oxidase to form DOPEG. However, there are qualitative and quantitative differences in the metabolic profile of the overflow evoked by various agonists. It is suggested that these differences could arise from their additional properties, such as their effect on the neuronal uptake process and (or) their ability to act as substrate for neuronal monoamine oxidase.Key words: noradrenaline, vas deferens, histamine, histamine H1 and H2 agonists.

Recent studies of the actions of cholinomimetic drugs on adrenergic nerves and their implications for the cholinergic link hypothesis

1980 ◽  
Vol 58 (1) ◽  
pp. 1-6 ◽  
Author(s):  
S. Jayasundar ◽  
M. M. Vohra
Keyword(s):  
Nerve Terminal ◽  
Physiological Function ◽  
Pharmacological Action ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Adrenergic Nerve Terminals ◽  
Adrenergic Neurotransmission ◽  
Na Release ◽  
Cholinomimetic Drugs ◽  
Adrenergic Neurone

This review analyzes the results of recent studies of the actions of cholinomimetic drugs on adrenergic nerve terminals and their implications for the cholinergic link hypothesis. Thus far, evidence suggests that the only possible action of endogenous acetylcholine (ACh) present near noradrenaline (NA) stores is an inhibition of the release of NA from the adrenergic nerve terminals and that NA is released only when the action of acetylcholinesterase in inhibited. Nicotinic agents have been shown to act on adrenergic nerve terminal membranes, a finding that casts doubt on the proposed intraneuronal cholinergic sites for the action of endogenous ACh. Evidence also indicates that the mode of adrenergic neurone blocking action of bretylium and guanethidine is independent of the proposed cholinergic process in NA release. Current findings do not support the proposal that nicotinic agents in higher concentrations interfere with adrenergic neurotransmission. It is therefore concluded that nicotinic agents, in causing the release of NA from adrenergic nerve terminals, are merely exhibiting a pharmacological action and not mimicking the physiological function of ACh, as proposed by the cholinergic link hypothesis.

Effect of subarachnoid hemorrhage on contractile responses and noradrenaline release evoked in cat cerebral arteries by histamine

1981 ◽  
Vol 55 (4) ◽  
pp. 543-549 ◽  
Author(s):  
Ramiro D. Lobato ◽  
Jesús Marín ◽  
Mercedes Salaices ◽  
Mercedes L. Rico ◽  
Carlos F. Sanchez
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Noradrenaline Release ◽  
Cerebral Arteries ◽  
Adrenergic Nerve ◽  
Contractile Responses ◽  
Content Type ◽  
Adrenergic Nerve Endings ◽  
Cervical Ganglia ◽  
6 Hydroxydopamine ◽  
Fine Print

✓ This study analyzes the changes induced by subarachnoid hemorrhage (SAH) on the contractile responses and the noradrenaline release evoked in cat cerebral arteries by histamine. The dose-dependent vasoconstriction induced by histamine on the cerebral arteries of normal cats was significantly reduced by diphenhydramine and phentolamine. When SAH was produced 3 and 7 days before the experiment, the histamine-induced vasoconstriction also decreased. Thereafter, a tendency to normalization in the contractile vascular responses was observed such that 15 days after the hemorrhage it was not significantly different from that found in control animals. The decrease in the contractile responses to histamine provoked by SAH was similar to that seen after pretreatment with intracisternal injections of 6-hydroxy-dopamine. The amount of radioactivity released by histamine following preincubation with 3H-noradrenaline from the cerebral arteries of cats exposed to SAH 3, 7, and 15 days before the experiment was significantly reduced when compared with controls. Moreover, the basal level of tritium release and the radioactivity retained at the end of the experiment were also decreased after SAH. These decreases were less marked 15 days after SAH. Intracisternal injections of 6-hydroxydopamine 3, 7, and 15 days prior to the assay, and the removal of both superior cervical ganglia 15 days before the experiment, also markedly reduced these three parameters. These results indicate that histamine releases noradrenaline from cat cerebral arteries, and SAH produces a transient denervation of the perivascular adrenergic nerve endings. The inhibition of the histamine-induced vasoconstriction observed after SAH might be explained by the impairment of the indirect adrenergic mechanism involved in the overall contractile response elicited by this amine in cerebral arteries. According to the present findings, histamine does not seem to play a significant role in the production of the cerebral vasospasm occurring after SAH.

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