Action of a β-bungarotoxin on autonomic ganglia and adrenergic neurotransmission

1977 ◽  
Vol 55 (3) ◽  
pp. 574-584 ◽  
Author(s):  
A. C. Kato ◽  
J. E. B. Pinto ◽  
M. Glavinović ◽  
B. Collier
Keyword(s):  
Nerve Stimulation ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Ach Release ◽  
Selective Binding ◽  
Release Of Noradrenaline ◽  
Cholinergic Nerve ◽  
Cholinergic Nerve Terminals ◽  
Adrenergic Nerve Terminals ◽  
Adrenergic Neurotransmission

A β-bungarotoxin was isolated from the venom of Bungarus multicinctus by column chromatography on Sephadex G-50 and SP-Sephadex. The toxin produced presynaptic effects on neuromuscular transmission with characteristics similar to those described by others. In a sympathetic ganglion, the toxin increased spontaneous acetylcholine (ACh) release and decreased ACh release evoked by preganglionic nerve stimulation. The toxin did not block the response of isolated ileum to cholinergic nerve stimulation, did not block the release of noradrenaline from the adrenergic nerve terminals of a nictitating membrane preparation, and did not alter the responses of smooth and cardiac muscle preparations to noradrenaline. It is suggested that the specificity of β-bungarotoxin for certain nerve terminals is related either to selective binding of the toxin or to the selective presence of a necessary substrate for its action. An attempt to show selective binding of 125I-toxin to cholinergic nerve terminals in skeletal muscle was not successful.

Stimulating actions of various prostaglandins and noradrenaline in strips of rabbit renal artery

1978 ◽  
Vol 56 (2) ◽  
pp. 321-323 ◽  
Author(s):  
F. Rioux ◽  
G. Gagnon ◽  
D. Regoli
Keyword(s):  
Renal Artery ◽  
Renal Arteries ◽  
Adrenergic Nerve ◽  
Prostaglandin E ◽  
Physiological Salt Solution ◽  
Nerve Terminals ◽  
Release Of Noradrenaline ◽  
Vasoconstrictor Effect ◽  
Adrenergic Nerve Terminals ◽  
Prostaglandins E

The myotropic effects of prostaglandins E1, E2, F2α, A1, and noradrenaline were evaluated in spirally cut strips of rabbit renal arteries suspended in a physiological salt solution maintained at 37 °C. The four prostaglandins as well as noradrenaline elicited contractions of the isolated rabbit renal artery. At concentrations higher than 1.0 × 10−7 g ml−1 the contracting effect of prostaglandin E1 diminished. The vasoconstrictor actions of prostaglandins E2 and F2α were potentiated by cocaine and inhibited by phentolamine. On the other hand, phentolamine did not inhibit the vasoconstrictor effect of prostaglandins E2 and F2α on strips of rabbit renal arteries removed from rabbits pretreated with reserpine. These results were taken as an indication that part of the contractile effects of prostaglandins E2 and F2α on the isolated rabbit renal artery may be due to the release of noradrenaline from adrenergic nerve terminals.

Adrenergic neuron blocking action of dehydrocorydaline isolated from Corydalis bulbosa

1976 ◽  
Vol 54 (3) ◽  
pp. 287-293 ◽  
Author(s):  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Pulmonary Artery ◽  
Nerve Stimulation ◽  
Inhibitory Action ◽  
Adrenergic Nerve ◽  
Active Principle ◽  
Nerve Terminals ◽  
Inhibitory Effects ◽  
Electrical Nerve Stimulation ◽  
Adrenergic Neuron ◽  
Adrenergic Nerve Terminals

Dehydrocorydaline, an active principle of Corydalis bulbosa alkaloids, in concentrations of 10−5M to 5 × 10−5M inhibited relaxation and the concomitant release of [3H]-noradrenaline caused by 10−4M nicotine and electrical perivascular nerve stimulation in the taenia caecum of guinea pig. The same inhibitory effects were observed on contraction and release of [3H]noradrenaline in the sympathetic nerve – pulmonary artery preparation of rabbit. On the other hand, neither relaxation nor contraction caused by exogenously applied noradrenaline was affected. These results suggest that the inhibitory action of dehydrocorydaline on the relaxation or contraction, produced by nicotine and electrical nerve stimulation, is due to blockade of noradrenaline release from the adrenergic nerve terminals in both the taenia caecum and pulmonary artery. Participation of the adrenergic neuron blocking action of dehydrocorydaline in preventing experimental ulceration is discussed.

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.

The calcium–magnesium interaction in the process of release of noradrenaline by nicotine

1977 ◽  
Vol 55 (6) ◽  
pp. 1383-1386 ◽  
Author(s):  
S. Jayasundar ◽  
M. M. Vohra
Keyword(s):  
Vas Deferens ◽  
Inhibitory Effect ◽  
Adrenergic Nerve ◽  
Neuronal Membrane ◽  
Nerve Terminals ◽  
Release Of Noradrenaline ◽  
Calcium Magnesium ◽  
Adrenergic Nerve Terminals ◽  
Dose Dependent

The calcium–magnesium (Ca2+–Mg2+) interaction in the process of nicotine-induced release of [3H]noradrenaline ([3H]NA) from rat isolated vas deferens was studied. Increasing extracellular concentrations of Mg2+ caused a dose-dependent depression of release of [3H]NA by nicotine, and this inhibitory effect of Mg2+ was overcome by raising the concentration of Ca2+. It is concluded that Mg2+ antagonizes the nicotine-induced increase in the Ca2+ influx into the adrenergic nerve terminals, and that nicotine acts on adrenergic neuronal membrane rather than intraneuronally to cause release of NA.

Prejunctional cholinergic modulation of adrenergic neurotransmission in the cardiovascular system

1980 ◽  
Vol 238 (3) ◽  
pp. H275-H281 ◽  
Author(s):  
P. M. Vanhoutte ◽  
M. N. Levy
Keyword(s):  
Inhibitory Effect ◽  
Autonomic Nerve ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Vascular Muscle ◽  
Adrenergic Nerve Terminals ◽  
Adrenergic Neurotransmission ◽  
Autonomic Nerve Terminals ◽  
Vascular Muscle Cells ◽  
Cholinergic Neurotransmitter

In the heart and in the blood vessel walls, complex adrenergic-cholinergic interactions occur both prejunctionally, at the level of the autonomic nerve terminals, and postjunctionally, at the level of the responding cells themselves. The principal prejunctional interaction appears to be an inhibition of the release of norepinephrine from adrenergic nerve terminals by the acetylcholine liberated from nearby cholinergic nerve endings. This inhibitory effect is mediated by muscarinic receptors located on the postganglionic sympathetic nerve terminals. The inhibitory effect of acetylcholine on cardiac and vascular tissues are therefore achieved in part by a direct influence of the cholinergic neurotransmitter on the cardiac and vascular muscle cells, and in part by an indirect influence on sympathetic neurotransmission.

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