Evidence against the participation of acetylcholine in transmission at sympathetic 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.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y78-047 ◽

1978 ◽

Vol 56 (2) ◽

pp. 321-323 ◽

Cited By ~ 3

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.

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Adrenergic neuron blocking action of dehydrocorydaline isolated from Corydalis bulbosa

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y76-042 ◽

1976 ◽

Vol 54 (3) ◽

pp. 287-293 ◽

Cited By ~ 11

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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