α1- and α2-adrenoceptor activation increases plasma glucagon levels in the mouse

Skoglund, Gunnar; Lundquist, Ingmar; Åhrén, Bo

doi:10.1016/0014-2999(87)90737-0

Cited by 30 publications

(16 citation statements)

References 29 publications

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“…CCK-8 was injected at the dose level of 6.3 nmol/kg. a dose level that is maximal with regard to stimulation of insulin and glucagon secretion [15,16], and terbutaline was injected at the dose level of 3.6 pmol/kg, a dose level that is maximal with regard to stimulation of glucagon secretion [17] and half-maximal with regard to stimulation of insulin secretion [18]. Blood samples were taken from the retrobulbar venous plexus [ 19,20] at 2 or 5.5 min after the intravenous injection.…”

Section: Methodsmentioning

confidence: 99%

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Lindskog¹,

Åhrén

1988

Horm Res

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The effects of the two intrapancreatic peptides galanin and pancreastatin on basal and stimulated insulin and glucagon secretion in the mouse were compared. It was found that at 2 min after intravenous injection of galanin or pancreastatin (4.0 nmol/kg), basal plasma glucagon and glucose levels were slightly elevated. Galanin was more potent than pancreastatin to elevate basal plasma glucagon levels: they increased from 60 ± 15 to 145 ± 19 pg/ml (p < 0.01) after galanin compared to from 35 ± 5 to 55 ± 8 pg/ml (p < 0.05) after pancreastatin. Plasma insulin levels were lowered by galanin (p < 0.05), but not by pancreastatin. CCK-8 (6.3 nmol/kg) or terbutaline (3.6 µmol/kg) markedly increased the plasma insulin levels. Galanin (4.0 nmol/kg) completely abolished the insulin response to CCK-8 (p < 0.001), but pancreastatin (4.0 nmol/kg) was without effect. Galanin inhibited the insulin response to terbutaline by approximately 60% (p < 0.01), but pancreastatin inhibited the insulin response to terbutaline by approximately 35% only (p < 0.05). CCK-8 and terbutaline did both elevate plasma glucagon levels by moderate potencies: neither pancreastatin nor galanin could affect these responses. Thus, in the mouse, galanin and pancreastatin both inhibit basal and stimulated insulin secretion, and stimulate basal glucagon secretion. Galanin is thereby more potent than pancreastatin. The study also showed that galanin potently inhibits insulin secretion stimulated by the octapeptide of cholecystokin and by the β2-adrenoceptor agonist terbutaline, and that pancreastatin inhibits terbutaline-induced insulin secretion.

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Section: Methodsmentioning

confidence: 99%

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Lindskog¹,

Åhrén

1988

Horm Res

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“…The mechanisms behind the gastrectomy-induced failure of glucose to suppress glucagon secretion in vivo is less clear. An increased activity in gastrectomized mice of adrenegic nerves innervating the glucagon-producing á_cells (Lundquist & Ericsson, 1978) might be a possible explanation, since catecholamines are known to potently stimulate glucagon secretion in mice (Skoglund et al 1987). Moreover, insulin is reportedly a powerful inhibitor of glucagon release (Maruyama et al 1984) and it is possible that the difference between gastrectomized and intact mice with respect to the in vivo glucagon response can be explained by differences in the amount of insulin released by glucose, since there was a marked impairment, both in vivo and in vitro, of glucose-induced insulin release in gastrectomized animals.…”

Section: Glucagon Secretionmentioning

confidence: 99%

Gastrectomy induces impaired insulin and glucagon secretion: evidence for a gastro‐insular axis in mice

Salehi

Chen

Håkanson

et al. 1999

The Journal of Physiology

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Hormones released from the digestive tract have been suggested to contribute to the metabolic disposal of ingested glucose. Thus, an oral glucose load is metabolized more rapidly than an intravenous glucose load, and more insulin is secreted after oral glucose than after an equivalent intravenous glucose load (McIntyre et al. 1964;Dupr e, 1991; Creutzfeldt & Nauck, 1992). Several intestinal hormones, including glucagon-like peptide_1-(7-36)-amide (GLP_1) and glucose-dependent insulinotrophic peptide (GIP), are thought to affect blood glucose by modulating the secretion of insulin and glucagon (Dupr e, 1991; Creutzfeldt & Nauck, 1992;Holst, 1994). However, the dysfunction of such intestinal hormone systems does not explain the alimentary hyperglycaemia often noted in patients who have undergone gastric surgery (Muir, 1949;Tobe et al. 1967). The possible existence of a gastro-insular axis prompted us to study the effect of gastrectomy in mice on the insulin and glucagon responses in vivo and in vitro to the three major types of regulators of islet hormone release, i.e. glucose (nutrient regulator), carbachol (phospholipase C regulator) and isobutylmethylxanthine (IBMX) or forskolin (cyclic AMP regulators). In addition, we tested the effect of a crude oxyntic mucosal extract on islet hormone release. We also monitored blood lipids since recent studies have indicated that free fatty acids may impair insulin release (Prentki & Corkey, 1996).

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“…They were subsequently demonstrated in vascular smooth muscle in which they subserve vasoconstriction, resulting in a pressor response in intact animals (Docherty et al, 1979;Drew & Whiting, 1979;Timmermans et al, 1979;Timmermans & Van Zwieten, 1980), and contraction in isolated preparations of certain blood vessels (Medgett et al, 1981;Holtz et al, 1982;Hicks et al, 1983). Recently a number of authors have shown that postjunctional a2-adrenoceptors are involved in several physiological functions in various tissues (Berridge et al, 1983;Reid, 1985; Strandhoy, 1985;Skoglund et al, 1987).…”

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confidence: 99%

α₂‐Adrenoceptor agonists enhance responses to certain other vasoconstrictor agonists in the rat tail artery

Xiao¹,

Rand²

1989

British J Pharmacology

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1 The effects of the a2-adrenoceptor agonists clonidine, rilmenidine, TL99 and UK14304 on the vasoconstrictor response to sympathetic nerve stimulation and on the concentration-response curves to noradrenaline and phenylephrine were compared in two isolated, perfused vascular tissues: the rat tail artery (which has both postjunctional al-and a2-adrenoceptors), and the rabbit ear artery (in which only cx-adrenoceptors are present postjunctionally). 2 In the rabbit ear artery, the first observable effect of a2-adrenoceptor agonists was inhibition of vasoconstrictor responses to sympathetic nerve stimulation. This occurred with concentrations of the M2-adrenoceptor agonists which were far below those producing vasoconstriction. Responses to noradrenaline were not affected. 3 In contrast, in the rat isolated perfused tail artery, a2-adrenoceptor agonists, in concentrations that produced no other observable effects, enhanced the vasoconstrictor responses to sympathetic nerve stimulation and to noradrenaline. Much higher concentrations of a2-adrenoceptor agonists produced vasoconstriction in most preparations and only then reduced the response to sympathetic nerve stimulation. The enhancing effect of CX2-adrenoceptor agonists was blocked by idazoxan, but not by prazosin.4 Vasoconstrictor responses in the rat tail artery to the relatively selective xl-adrenoceptor agonist phenylephrine were enhanced by X2-adrenoceptor agonists. The enhancement of the response to phenylephrine was greater than that to the mixed a1-and a2-adrenoceptor agonist noradrenaline. 5 Vasoconstrictor responses in the rat tail artery to vasopressin, ATP and KCl, like those to a1-adrenoceptor agonists, were enhanced by a2-adrenoceptor agonists. However, vasoconstrictor responses to 5-hydroxytryptamine and angiotensin II were not enhanced.

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α1- and α2-adrenoceptor activation increases plasma glucagon levels in the mouse

Cited by 30 publications

References 29 publications

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Gastrectomy induces impaired insulin and glucagon secretion: evidence for a gastro‐insular axis in mice

α₂‐Adrenoceptor agonists enhance responses to certain other vasoconstrictor agonists in the rat tail artery

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α1- and α2-adrenoceptor activation increases plasma glucagon levels in the mouse

Cited by 30 publications

References 29 publications

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Galanin and Pancreastatin Inhibit Stimulated Insulin Secretion in the Mouse: Comparison of Effects

Gastrectomy induces impaired insulin and glucagon secretion: evidence for a gastro‐insular axis in mice

α2‐Adrenoceptor agonists enhance responses to certain other vasoconstrictor agonists in the rat tail artery

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α₂‐Adrenoceptor agonists enhance responses to certain other vasoconstrictor agonists in the rat tail artery