Histaminergic Stimulation of Prolactin Secretion Mediated via H&lt;sub&gt;1&lt;/sub&gt;- or H&lt;sub&gt;2&lt;/sub&gt;-Receptors: Dependence on Routes of Administration

Knigge, Ulrich; Matzen, Steen Henrik; Warberg, Jørgen

doi:10.1159/000124619

Cited by 28 publications

(29 citation statements)

References 20 publications

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“…Insufficient dose or incorrect administration of 2-TEA can be excluded as the compound increased ACTH secretion to a level identical to that of HA and to a level previously observed [5]. However, our present result in conscious rats is in accordance with our previous finding that the H 1 receptor agonist did not affect PRL secretion in urethane-anesthetized animals [4]. Further studies are required in order to establish a role of H 1 receptors in the mediation of histaminergic activation of PRL secretion.…”

Section: Discussionsupporting

confidence: 92%

“…The ACTH antiserum (generously provided by the National Pituitary Agency, National Institute of Health) does not cross-react with β-endorphin or β-LPH and has less than 0.4% cross-reactivity with α- and β-melanocyte stimulating hormone. Synthetic human ACTH [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39](generously provided by the National Pituitary Agency, National Institute of Health) served as reference preparation and iodination. The least detectable quantity of ACTH was 1 pmol/l plasma, and the intra- and interassay coefficients of variation were 4 and 5%.…”

Section: Methodsmentioning

confidence: 99%

“…It has been shown that HA stimulates corticotropin (ACTH) secretion via activation of H 1 and H 2 receptors and prolactin (PRL) secretion predominantly via H 2 but also via H 1 receptors [4, 5, 6]. The effect of HA is indirectly exerted via activation of neuronal systems in the hypothalamus, which subsequently stimulate pituitary hormone secretion [7].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

et al. 1999

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We investigated the role of adrenergic receptors in histamine (HA)-induced release of corticotropin (ACTH) and prolactin (PRL) in conscious male rats. Specific α- or β-receptor antagonists were administered intracerebroventricularly in doses of 1 mmol at time –20 min, and HA (270 nmol), the H₁ receptor agonist 2-thiazolylethylamine (2-TEA; 2,180 nmol) or the H₂ receptor agonist 4-methylHA (4-MeHA; 790 nmol) were administered intracerebroventricularly at –15 min. The animals were decapitated at 0 min, and plasma was analyzed for ACTH and PRL. Administration of HA and the histaminergic agonists stimulated ACTH secretion equally, while only HA and the H₂ receptor agonist stimulated PRL secretion. Pretreatment with the adrenergic receptor antagonists had no effect on the ACTH response to the histaminergic compounds. In contrast, the PRL response to HA or 4-MeHA was inhibited or prevented by the α-receptor antagonists phenoxybenzamine and phentolamine, the α₁-receptor antagonist prazocin, the β-receptor antagonist propranolol and the β₁-receptor antagonist atenolol, whereas the α₂-receptor antagonist yohimbine or the β₂-receptor antagonist ICI-118-551 had no effect. The study indicates that histaminergic neurons interact with the catecholaminergic neuronal system in regulation of PRL secretion, and that this interaction is dependent upon activation of α₁- and β₁-receptors. In contrast, histaminergic neurons stimulate ACTH secretion independently of adrenergic receptor activation.

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

et al. 1999

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“…Furthermore, histaminergic neurons, which originate exclusively in the posterior hypothalamus (1), seem to be involved in the mediation of stressinduced release of these hormones (2). Since HA does not appear to stimulate ACTH/b-endorphin (3,4) or prolactin secretion (5,6) directly at the pituitary level, its action may be indirect via activation of hypothalamic neurons, which subsequently release hypophysiotropic factors which stimulate pituitary hormone secretion. Corticotropin-releasing hormone (CRH) as well as arginine-vasopressin (AVP) and oxytocin (OT) are involved in regulation of ACTH and b-endorphin (7,8) secretion, and AVP and OT are also involved in control of prolactin secretion (9).…”

Section: Introductionmentioning

confidence: 99%

Neuronal histamine and expression of corticotropin-releasing hormone, vasopressin and oxytocin in the hypothalamus: relative importance of H1 and H2 receptors

Kjær¹,

Larsen

Knigge³

et al. 1998

European Journal of Endocrinology

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Centrally administered histamine (HA) stimulates the secretion of the pro-opiomelanocortin-derived peptides ACTH and b-endorphin as well as prolactin. The effect of HA on secretion of these adenohypophysial hormones is indirect and may involve activation of hypothalamic neurons containing corticotropin-releasing hormone (CRH), arginine-vasopressin (AVP) or oxytocin (OT).We studied the effect of activating central HA receptors by central infusion of HA, HA agonists or antagonists on expression of CRH, AVP and OT mRNA in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei.Intracerebroventricular infusion of HA (270 nmol), the H 1 -receptor agonist 2-thiazolylethylamine or the H 2 -receptor agonist 4-methylhistamine increased the level of CRH mRNA in the PVN, and OT mRNA in the SON. In contrast, none of these compounds had any effect on expression of AVP mRNA in the PVN or SON. Administration of the H 1 -receptor antagonist mepyramine or the H 2 -receptor antagonist cimetidine had no effect on basal expression of CRH, AVP or OT mRNA in the PVN and/or SON except for a slight inhibitory effect of cimetidine on CRH mRNA expression in the PVN. Pretreatment with mepyramine or cimetidine before HA administration inhibited the HA-induced increase in OT mRNA levels but had no effect on the HA-induced increase in CRH mRNA levels in the PVN.We conclude that HA stimulates hypothalamic CRH and OT neurons by increasing mRNA levels, and this effect seems to be mediated via activation of both HA H 1 and H 2 receptors.

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“…At time 0, the rats were decapitated and trunk blood was collected for measurement of PRA. Decapitation took place between 10.00 and 12.00 h. The doses of antagonists were chosen on the basis of previous studies where they effectively antagonized HA-induced prolactin and ACTH secretion [15, 16]. …”

Section: Methodsmentioning

confidence: 99%

Dehydration-Induced Renin Secretion: Involvement of Histaminergic Neurons

Kjær

Knigge²,

Jørgensen³

et al. 1998

Neuroendocrinology

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Renin secretion is controlled locally in the kidneys as well as via central neuronal mechanisms. The neuronal mechanisms are not fully understood but may involve the neurotransmitter histamine (HA) since centrally infused HA stimulates renin secretion. This, however, does not prove that HA is of any physiological importance for the regulation of renin secretion. Dehydration is a physiological stimulus of renin secretion and, therefore, we studied the possible role of hypothalamic histaminergic neurons in dehydration-induced renin secretion in conscious male rats. In addition, we expanded on our previous investigations of HA-induced renin secretion. Twenty-four hours of dehydration induced a 3-fold increase in plasma renin activity (PRA). Pretreatment with the HA synthesis inhibitor α-fluoromethylhistidine inhibited the dehydration-induced PRA secretion by 80% whereas pretreatment with the H₁ receptor antagonist mepyramine (MEP) or the H₂ receptor antagonist ranitidine (RAN) inhibited the PRA response to dehydration by approximately 40%. In euhydrated control rats, none of the HA-blocking agents had any significant effect on basal PRA secretion. Central administration of HA stimulated PRA almost 2-fold and the maximum concentration of PRA was reached after 15 min. Pretreatment with the H₁ receptor antagonist MEP or the H₂ receptor antagonist RAN totally inhibited the HA-induced PRA secretion. We conclude that HA activates renin secretion via H₁ and H₂ receptors and that HA seems to be a physiological mediator of dehydration-induced renin secretion via activation of H₁ and H₂ receptors. The effect is probably indirect and may among others involve the catecholaminergic and serotonergic systems.

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Histaminergic Stimulation of Prolactin Secretion Mediated via H<sub>1</sub>- or H<sub>2</sub>-Receptors: Dependence on Routes of Administration

Cited by 28 publications

References 20 publications

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

Effect of Selective Blockade of Catecholaminergic Alpha and Beta Receptors on Histamine-Induced Release of Corticotropin and Prolactin

Neuronal histamine and expression of corticotropin-releasing hormone, vasopressin and oxytocin in the hypothalamus: relative importance of H1 and H2 receptors

Dehydration-Induced Renin Secretion: Involvement of Histaminergic Neurons

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