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.

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.

Inhibition by dopamine of the stimulation-induced efflux of [3H]noradrenaline in renal arteries: limitations of the unitary hypothesis of presynaptic regulation of transmitter release

1980 ◽  
Vol 58 (5) ◽  
pp. 504-512 ◽  
Author(s):  
Stanley Kalsner ◽  
Chi-Chung Chan
Keyword(s):  
Transmitter Release ◽  
Feedback Loop ◽  
Feedback System ◽  
Renal Arteries ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Adrenergic Nerve Terminals ◽  
Presynaptic Regulation ◽  
Sympathetic Nerve Activation ◽  
Frequency Of Stimulation

The supposition was tested that a pattern of agonist inhibition of 3H-labelled transmitter efflux which shows a decline in intensity as the frequency of stimulation rises provides major evidence for the existence of a functional autoinhibitory feedback loop mediated by released transmitter and located on adrenergic nerve terminals. For these experiments dopamine was used, as it is not released in significant quantities in the ordinary course of sympathetic nerve activation and it appears to act presynaptically in several tested tissues at a locus discrete from that acted on by noradrenaline. Dopamine (3 × 10−7 and 3 × 10−6 M) inhibited the stimulation-induced efflux of [3H]noradrenaline from cattle renal arteries and did so to a declining extent with increasing frequency (1–15 Hz). Known antagonists of dopamine action, pimozide and metoclopromide, antagonized this effect of dopamine but did not by themselves enhance stimulation-induced transmitter efflux or block the inhibiting effects of exogenous noradrenaline on efflux, establishing the specificity of dopamine action in renal artery and indicating the absence of an operative negative feedback loop mediated by dopamine. This interpretation was substantiated by the finding that although dopamine reduced the magnitude of contractile responses to nerve stimulation neither pimozide nor metoclopromide enhanced the amplitude of nerve-induced contractions. It thus appears that a pattern of agonist effect on transmitter efflux which manifests a diminution in intensity as the frequency of stimulation climbs is not derived from the operation of an ongoing autoinhibitory feedback system regulating transmitter release but by a yet to be established factor.

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.

Ionomycin stimulates secretion of catecholamines from cat adrenal gland and spleen

1982 ◽  
Vol 242 (3) ◽  
pp. E137-E145 ◽  
Author(s):  
M. H. Carvalho ◽  
J. C. Prat ◽  
A. G. Garcia ◽  
S. M. Kirpekar
Keyword(s):  
Chromaffin Cells ◽  
Adrenal Glands ◽  
Secretory Response ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Potassium Depolarization ◽  
Calcium Dependent ◽  
Dopamine Beta Hydroxylase ◽  
Adequate Stimulus ◽  
Adrenergic Nerve Terminals

Ionomycin, a polyether antibiotic, stimulated the secretion of catecholamines and dopamine beta-hydroxylase from perfused adrenal glands and [3H]norepinephrine ([3H]NE) from spleens of the cat. Release was calcium dependent, and strontium or barium did not substitute for calcium. Ionomycin failed to release [3H]NE from reserpinized spleens. High magnesium did not interfere in the ionomycin response, but lanthanum and manganese blocked it. Ionomycin response that was pH dependent was not affected by potassium depolarization. The secretory response to ionomycin was enhanced when both glycolysis and oxidative metabolism were inhibited. It is concluded that ionomycin introduces calcium into the chromaffin cells and adrenergic nerve terminals to cause the secretory response and that a rise in intracellular calcium may be an adequate stimulus for secretion.

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.

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