Evidence for Noradrenaline and Adrenaline as Sympathetic Transmitters in the Chicken

DeSANTIS, V.P.; Längsfeld, W.; Lindmar, R.; Löffelholz, K.

doi:10.1111/j.1476-5381.1975.tb06937.x

Cited by 39 publications

(11 citation statements)

References 16 publications

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“…The findings that adrenaline is present in a higher concentration in the fowl rectum suggest that this catecholamine may act as a neurotransmitter in the adrenergic fibres in the rectum of this species. This agrees with the recent observation that both noradrenaline and adrenaline act as sympathetic neurotransmitters in the fowl heart and spleen (DeSantis et al, 1975).…”

Section: Discussionsupporting

confidence: 93%

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Evidence That Adrenaline Is Released From Adrenergic Neurones in the Rectum of the Fowl

Komori

Ohashi

Okada

et al. 1979

British Journal of Pharmacology

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The rectum isolated from the fowl was perfused with Tyrode solution via the caudal mesenteric artery. Noradrenaline and adrenaline were biologically or fluorimetrically assayed in perfusates collected before and during stimulation of Remak's nerve or of the periarterial nerves. Perfusates collected during nerve stimulation relaxed the chick rectum and rat stomach strips which served as assay tissues. This effect was attributed to the action of noradrenaline or adrenaline released from adrenergic nerve endings which appeared in the perfusates. Perfusates obtained during stimulation (30 Hz for 60 s) of Remak's nerve contained both noradrenaline and adrenaline when measured fluorimetrically. The mean output per stimulus train was 0.8 ± 0.2 ng/g wet wt. tissue for noradrenaline and 1.7 ± 0.2 ng/g wet wt. tissue for adrenaline (n = 7). Perfusates obtained during stimulation (30 Hz for 60 s) of the periarterial nerves contained noradrenaline in a concentration of 1.6 ± 0.3 ng/g wet wt. tissue per stimulus train, but almost no adrenaline (n = 7). Neither stimulation of Remak's nerve nor the periarterial nerves liberated catecholamines when the rectum was perfused with Tyrode solution containing low Ca2+ (0.1 mm) and high Mg2+ (10 mm). Infusion of high potassium solution (50 mm) increased markedly the output of noradrenaline and adrenaline. Adrenaline as well as noradrenaline may function as the adrenergic neurotransmitter in the rectum of the fowl.

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Section: Discussionsupporting

confidence: 93%

“…This agrees with the recent observation that both noradrenaline and adrenaline act as sympathetic neurotransmitters in the fowl heart and spleen (DeSantis et al, 1975).…”

Section: Discussionsupporting

confidence: 82%

Evidence That Adrenaline Is Released From Adrenergic Neurones in the Rectum of the Fowl

Komori

Ohashi

Okada

et al. 1979

British Journal of Pharmacology

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“…Circulating NE and E in birds originate from adrenal chromaffin cells and sympathetic nerve endings [10]. Therefore, the large increase observed in circulating catecholamine levels following the injection of glucagon may indicate an activation of the sympatho-adrenal system, thereby supporting an indirect effect of glucagon on skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the catecholaminergic system in glucagon-induced thermogenesis in Muscovy ducklings ( Cairina moschata )

Filali-Zegzouti

Abdelmelek

Rouanet

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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Physiological studies have shown that glucagon is a potential mediator of nonshivering thermogenesis (NST) in birds. The present work was undertaken in order to investigate whether the observed thermogenesis results from a direct action of glucagon on avian thermoregulatory mechanisms or in fact requires the participation of other agents such as catecholamines. Our experiments were performed using cold-acclimated (CA) ducklings which developed muscle NST. A comparison was made with thermoneutral (TN) ducklings of the same age. Our principal results showed that: (1) at ambient temperature (25 degrees C), circulating norepinephrine (NE) was markedly decreased in CA ducklings (-42%), while circulating epinephrine (E) did not undergo any consistent change; (2) in CA and TN ducklings, an intraperitoneal injection of glucagon (360 microg x kg(-1)) was followed after 10 min by prominent lipolysis and a large increase in circulating NE (4- to 6-fold) and E (14- to 17-fold), which was sustained for at least 1 h. The elevation of circulating NE was less pronounced in CA ducklings. The thermogenic action of glucagon in birds is probably indirect and involves at least the mobilization of lipids and sympatho-adrenal stimulation. The changes in peripheral noradrenergic activity during cold acclimation could be associated with adaptive changes leading to NST.

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“…This suggests that in fetal sheep the increase in circulating plasma catecholamines in response to hypoxemia is primarily of adrenal medullary origin. In the adult chicken, epinephrine and norepinephrine are secreted as sympathetic neurotransmitters (8), suggesting that, in the adult chicken, postganglionic sympathetic nerve stimulation might make a greater contribution to the plasma concentrations of epinephrine and norepinephrine. The contribution of neuronal spillover to circulating plasma concentrations of catecholamines is unknown for the chick embryo.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo

Mulder

Miedema

Mey

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of the heart and brain. Peripheral vasoconstriction contributes to this response and is partly mediated by the release of catecholamines. Two mechanisms of catecholamine release in the fetus are reported: 1) neurogenic sympathetic stimulation and 2) a nonneurogenic mechanism via a direct effect of hypoxemia on chromaffin tissues. In the present study, the effects of sympathetic blockade on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia were studied in the chick embryo at different stages of incubation. Only at the end of the incubation period, sympathetic blockade markedly attenuated the increase in plasma catecholamine concentrations and resulted in a greater fraction of the cardiac output distributed to the carcass. However, these effects did not prevent a significant increase in cardiac output to the brain and heart during acute hypoxemia. These data imply that in the chick embryo the contribution of neurogenic mechanisms to the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period. fetus; hexamethonium; hypoxia; catecholamines; avian HYPOXEMIA IN THE FETUS, resulting largely from placental dysfunction or umbilical blood flow impairment, has been postulated to be a major cause of neurological damage and neonatal morbidity (20,30). During gestation, fetal cardiovascular responses develop to maintain organ blood flow and minimize damage of sensitive tissues during episodes of hypoxemia (for review see Refs. 11,12,and 14). The mechanisms mediating the fetal cardiovascular response to hypoxemia are triggered by carotid chemoreceptor stimulation, which elicits bradycardia, hypertension, and a redistribution of the cardiac output in favor of the adrenal gland, the heart, and the brain (10). Neural sympathetic stimulation and endocrine vasopressor substances, such as catecholamines, contribute to peripheral vasoconstriction, prioritizing the fetal cardiac output away from the periphery to the more vital organs (11,12,14). Previous studies from our laboratory have demonstrated the importance of catecholamine release in the cardiovascular response to an episode of acute hypoxemia in the chick embryo. At the end of the incubation period, plasma concentrations of catecholamines increase markedly in response to acute hypoxemia (21), and treatment of the chick embryo with the ␣-adrenergic receptor antagonist phentolamine prevented the redistribution of the cardiac output away from the peripheral circulations (22).In fetal sheep (4, 5, 27) and neonatal rats (29), at least two mechanisms mediating catecholamine release in response to hypoxemia have been described. First, before functional innervation of the adrenal glands, hypoxemia may stimulate chromaffin cells directly to promote catecholamine release into the circulation. Second, after the establishment of innervation to the adrenal gland, hypoxemia may stimulate adren...

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Evidence for Noradrenaline and Adrenaline as Sympathetic Transmitters in the Chicken

Cited by 39 publications

References 16 publications

Evidence That Adrenaline Is Released From Adrenergic Neurones in the Rectum of the Fowl

Evidence That Adrenaline Is Released From Adrenergic Neurones in the Rectum of the Fowl

Involvement of the catecholaminergic system in glucagon-induced thermogenesis in Muscovy ducklings ( Cairina moschata )

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo

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