Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Be, Dunning; Jg, Verbalis; Cp, Fawcett

doi:10.1159/000124206

Cited by 20 publications

(7 citation statements)

References 13 publications

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“…This is in accordance with previous findings, which showed that a 15 -30% acute reduction in blood volume increased AVP (9, 52 -54), and OT concentration in peripheral (5,50,55) and pituitary portal plasma (56), and increased AVP content and mRNA in the hypothalamus (52,57,58). The OT response to hemorrhage seems to be mediated via 5-HT 2 receptors, since the response was inhibited by pretreatment with the 5-HT 2Cþ2A antagonist LY.…”

Section: Discussionsupporting

confidence: 93%

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Jørgensen

Knigge²,

Kjær³

et al. 2002

European Journal of Endocrinology

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Objective: To investigate the involvement of serotonin (5-hydroxytryptamine -5-HT) receptors in mediation of stress-induced arginine vasopressin (AVP) and oxytocin (OT) secretion in male rats. Design: Experiments on laboratory rats with control groups. Methods: Different stress paradigms were applied after pretreatment with intracerebroventricular infusion of saline or different 5-HT antagonists. Results: Restraint stress (5 min), hypotensive hemorrhage or dehydration for 24 h increased AVP secretion fivefold and OT secretion threefold. Swim stress for 3 min had no effect on AVP secretion, but increased OT secretion threefold. Ether vapor or hypoglycemia had no effect on AVP or OT secretion. The restraint stress-induced AVP response was inhibited by pretreatment with the 5-HT 2Aþ2C antagonists ketanserin (KET) and LY-53857 (LY) and the 5-HT 3þ4 antagonist ICS-205930 (ICS), whereas the 5-HT 1A antagonist WAY-100635 (WAY) had no effect. The OT response to restraint stress was inhibited by WAY, KET and LY but not by ICS. KET and LY inhibited OT response to dehydration, and LY inhibited OT response to hemorrhage. Neither of the antagonists affected AVP responses to dehydration or hemorrhage, nor the swim stress-induced OT response.

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Section: Discussionsupporting

confidence: 93%

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Jørgensen

Knigge²,

Kjær³

et al. 2002

European Journal of Endocrinology

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“…The characterization of this receptor at the molecular level in recent years has revealed that it is also abundantly expressed in the pancreas and that dDAVP, thought to be a selective V2 agonist, bound equally well to the V1b receptor [55]. Actually, a number of older studies have shown that vasopressin or dDAVP stimulates glucagon and insulin release in vivo, or in isolated perfused pancreas or in cultured cells from pancreatic origin [52, 56, 57, 58, 59]. It is thus conceivable that some of the effects observed in studies involving dDAVP administration may be due to an increase in glucagon-mediated direct and indirect effects on its main target organs, liver and kidney (fig.…”

Section: V1a and V1b Vasopressin Receptors In Diabetes Mellitusmentioning

confidence: 99%

Vasopressin and Diabetes mellitus

Bankir¹,

Bardoux²,

Ahloulay³

2001

Nephron

100

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In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the developement of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.

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“…Moreover, certain hypothalamic/pituitary peptides can influence both insulin and glucagon release. For example, vasopressin apparently potentiates the release of glucagon during hemorrhagic stress [45]. In addition, peptides released from islet cells may influence the secretions of other islet cell types in a paracrine manner.…”

Section: Criteria For Pancreatic Neuropeptidesmentioning

confidence: 99%

Neuropeptidergic versus cholinergic and adrenergic regulation of islet hormone secretion

1986

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The pancreatic islets are richly supplied with autonomic nerves. The fibres follow the arterioles, penetrate the islets and terminate close to the endocrine ceils. This morphological relationship makes it likely that the nerves are involved in the physiological regulation of islet function. A great number of papers have been published describing the effects of electrical stimulation of autonomic nerves and of presumed neurotransmitters and blocking agents on islet function. During the last decade several reviews have summarized these findings and dealt with various aspects of neuroregulation of islet hormone secretion [1][2][3][4]. In general, these reviews have attempted to explain the effects of neural activation upon islet function in terms of the known effects of the classical adrenergic and cholinergic neural inputs to the islets. However, recent studies suggest that peptidergic input may also be important. Therefore, in this review we will highlight the new studies of the neuroregulation of insulin, glucagon, somatostatin and pancreatic polypeptide secretion, and specifically emphasize the role of the neuropeptides, in addition to the classical neurotransmitters acetylcholine and noradrenaline, as potential mediators of these effects. Effects of vagal nerve stimulation and cholinergic agonists and antagonists on islet hormone secretionInsulin secretion. Electrical activation of the vagus has been shown to stimulate insulin secretion in several species, including dogs [7], calves [8] and pigs [9,10]. The response in dogs and calves is inhibited by atropine [7,8], implicating an interaction of the neurotransmitter acetylcholine with a post-ganglionic muscarinic receptor. However, in pigs atropine does not block the response, suggesting non-cholinergic, perhaps peptidergic, neurotransmission [9]. Neurotransmission at the ganglia is, however, mediated by a classical nicotinic action of acetylcholine, since hexamethonium blocks the response [9].Pharmacologic stimulation with the cholinergic agonists acetylcholine or Carbachol induces insulin secretion both in vitro [11] and in vivo [3,12]. Such stimulation could be due either to activation of nicotinic receptors on the intrapancreatic ganglia or to activation of muscarinic receptors on the B cells themselves. Since atropine blocks many of these responses, it appears that the vagus stimulates insulin secretion by a muscarinic mechanism in most circumstances. Cholinergic-islet interactions AnatomyThe preganglionic cholinergic nerves which innervate the pancreas originate in the dorsal motor nucleus of the vagus and in the nucleus ambiguus, travel in the vagus nerve and terminate at ganglia within the pancreas, sometimes within the islets [2]. These ganglia integrate neural signals and control the activity of the intrapancreatic postganglionic fibres which innervate individual endocrine cells. Though it was originally believed that all the post-ganglionic fibres within the pancreas were cholinergic, recent evidence suggests that some are peptidergic [5]. The import...

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Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Cited by 20 publications

References 13 publications

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Vasopressin and Diabetes mellitus

Neuropeptidergic versus cholinergic and adrenergic regulation of islet hormone secretion

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