The Effect of Adrenergic and Cholinergic Antagonists on Central Histaminergic Stimulation of Pituitary-Adrenocortical Response under Stress in Rats

Bugajski, J; Gadek, A

doi:10.1159/000123946

Cited by 19 publications

(16 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All compounds were dissolved in saline except Pra, which was dissolved in saline acidified with 0.1 N HCl and adjusted with 0.1 N NaOH to pH 7.4. The dose of 1 mmol used is approximately similar to the doses of adrenergic receptor antagonists previously found to affect stimulated ACTH and PRL secretion [25, 27, 28, 37, 38]. …”

Section: Methodsmentioning

confidence: 94%

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

et al. 1999

View full text Add to dashboard Cite

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.

show abstract

Section: Methodsmentioning

confidence: 94%

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

et al. 1999

View full text Add to dashboard Cite

show abstract

“…However, neither antagonist was effective in inhibiting the histamineinduced increase in plasma ACTH and corticosterone concentrations. On the contrary, Bugajski & Gadek (1983) reported that cimetidine and metiamide inhibited histamineinduced corticosterone increase. It seems likely that histamine-induced hormone secretion is mediated mainly through HI-receptor, and to a lesser extent through the H2-receptor.…”

Section: Discussionmentioning

confidence: 93%

“…histamine injection. On the other hand, Bugajski & Gadek (1983) demonstrated that in stressed rats, the corticosterone response to histamine is mediated by both H,-and H2-central receptors. Also, it has been reported that the H2-receptor is responsible for histamine-induced ACTH release in rats and man (Morita & Koyama, 1979;Knigge et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Effects of intracerebroventricular injection of histamine and related compounds on corticosterone release in rats

Tsujimoto

Okumura

Kamei

et al. 1993

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of intracerebroventricular (i.c.v.) injection of histamine and related compounds on plasma adrenocorticotrophic hormone (ACTH) and corticosterone concentrations were studied in conscious rats.2 Histamine at doses of 5-20 iLg kg-' rapidly increased plasma ACTH and corticosterone concentrations almost simultaneously, and subsequent courses were also similar to each other. However, in the case of , the plasma ACTH concentration first increased followed by an increase in plasma corticosterone concentration. Even in hypophysectomized rats, a significant increase in plasma corticosterone concentration was induced by histamine at doses of 20 and 50 iLg kg-'. 4 Both H,-agonist (2-methylhistamine) and H2-agonists (4-methylhistamine and impromidine) also induced similar effects to those of histamine. Pretreatment with pyrilamine caused an inhibition of histamine-induced increase in plasma ACTH and corticosterone concentrations, while both cimetidine and ranitidine failed to inhibit this effect. However, both H2-blockers were effective in inhibiting the 4-methylhistamine-induced elevation of plasma ACTH and corticosterone concentrations. 5 Neither (R)-ac-methylhistamine nor thioperamide had a significant effect, indicating that the H3-receptor is not involved in the histamine-induced increase in plasma ACTH and corticosterone concentrations. 6 From these findings, it was concluded that (1) electrical signals transmitted from the brain to the adrenal gland through the neurones may be involved in the rapid corticosterone release induced by histamine, and (2) not only H,-but also H2-receptors are implicated in histamine-induced hormone secretions in rats, though the contribution of the H2-receptor is less important than that of the HI-receptor.

show abstract

“…There is a high density of brain mast cells in regions situated at the boundary between the central nervous system (CNS) and its surroundings [such as in the circumventricular organs (8,17) and median eminence (38,41,42,53)]. Administration of histamine into the cerebral third ventricle (V III ) leads to increases in various stress hormones [such as ACTH-adrenocortical hormones (6,42,57,66) and catecholamines (16)] in the peripheral circulation. Histamine and its receptors are highly concentrated within the hypothalamus (4,6,40,57,59), and various types of stress induce significant alterations in both histamine synthesis and its concentration in several brain regions (5,57,59,63).…”

mentioning

confidence: 99%

“…Administration of histamine into the cerebral third ventricle (V III ) leads to increases in various stress hormones [such as ACTH-adrenocortical hormones (6,42,57,66) and catecholamines (16)] in the peripheral circulation. Histamine and its receptors are highly concentrated within the hypothalamus (4,6,40,57,59), and various types of stress induce significant alterations in both histamine synthesis and its concentration in several brain regions (5,57,59,63). Renin secretion is activated via the hypothalamic-sympathetic outflow during various forms of stress (1,14,60) and also during cardiovascular dysfunction (3,13,26,33,35,36,58).…”

mentioning

confidence: 99%

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Matsumoto¹,

Inoue²,

Shimada³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Because degranulation of brain mast cells activates adrenocortical secretion ( 41 , 42 ), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 μg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na+, K+, and Cl−), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H1histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H2histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 μg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).

show abstract

The Effect of Adrenergic and Cholinergic Antagonists on Central Histaminergic Stimulation of Pituitary-Adrenocortical Response under Stress in Rats

Cited by 19 publications

References 25 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

Effects of intracerebroventricular injection of histamine and related compounds on corticosterone release in rats

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

Contact Info

Product

Resources

About