H&lt;sub&gt;1&lt;/sub&gt;- and H&lt;sub&gt;2&lt;/sub&gt;-Histamine Receptor Antagonists and Induced Release of Prolactin in Male Rats

Donoso, Alfredo O.; Banzán, Arturo M.

doi:10.1159/000122967

Cited by 23 publications

(16 citation statements)

References 6 publications

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“…It was shown in a previous paper that the histamine-in duced prolactin release in male rats is blocked by Hz-antihistamine, metiamide [10]. The present results support this finding, and show in addition that ranitidine, a novel H2-histamine agonist [4], has a similar action.…”

Section: Discussionsupporting

confidence: 90%

“…In our experi ence [10; and the present results] both antihistamines, when given alone intraventricularly did not affect prolactin re lease. On the other hand, mepyramine as observed herein and previously [10] did not prevent the histamine effect. As is known, mepyramine is a potent Hi-antagonist [31].…”

Section: Discussionsupporting

confidence: 51%

“…The stimulatory effect of histamine on prolactin release [9,10], was further examined to define receptor mediation. As expected, plasma prolactin levels were significantly in- creased by 5 pg histamine ( fig.…”

Section: Effects Of Histamine and Histamine Agonists In Ether-anesthementioning

confidence: 99%

“…Hi-receptors are blocked by the classical antihistamines, and H2-receptors by a more recently developed group of antihis tamines [3,31], It was previously reported that the H2-histamine antago nist metiamide blocked the increase of plasma prolactin levReceived: September 17,1982 Accepted after revision: December 20, 1982 els induced by histamine in male rats [10], Furthermore, cimetidine, another ^-antagonist, was demonstrated to act similarly [29]. By contrast, the Hi-antagonists mepyramine and diphenhydramine, had no blocking effect [ 10,29]. It ap pears, therefore, that histamine might involve activation of H2-receptors to increase the release of prolactin.…”

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confidence: 99%

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Histamine-Induced Prolactin Release: Pharmacological Characterization of Receptors in Male Rats

Donoso¹,

Zárate²,

Seltzer³

1983

Neuroendocrinology

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Studies were undertaken to investigate the nature of receptors involved in the prolactin-releasing action of histamine in male rats. The increase of plasma prolactin levels induced by third-ventricle injection of histamine was blocked by intraventricular injection of ranitidine, an H2-antagonist, but not by systemic administration of mepyramine, an H₁-antagonist. The H2-histamine agonists 4-methylhistamine and Dimaprit, given intraventricularly in unrestrained and ether-anesthetized rats, enhanced prolactin release. The effect of 4-methylhistamine was dose-dependent, whereas Dimaprit had opposite effects depending on the dose. In low doses, Dimaprit decreased whereas in higher doses it increased plasma prolactin levels. The stimulatory effects of both agonists, similar to those produced by histamine itself, were blocked by metiamide (H2-antagonist), but not by intraventricular mepyramine. High doses of mepyramine only partially decreased the effects of 4-methylhistamine. Ranitidine was able to prevent the prolactin response to 4-methylhistamine. The selective H₁-histamine agonist 2,2-pyridylethylamine had no action on prolactin release. 2-Methylhistamine, which exhibits predominantly H₁-mediated actions, increased the release of prolactin. Its effect, however, was blocked by low doses of metiamide and was obtained at higher concentrations than 4-methylhistamine. Mepyramine prevented 2-methylhistamine action only at high doses. It is concluded that the increased release of prolactin evoked by histamine in male rats is mainly due to its action on H2-receptors. In addition, the results altogether indicate that H₁-receptors have not a significant participation.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 51%

Section: Effects Of Histamine and Histamine Agonists In Ether-anesthementioning

confidence: 99%

mentioning

confidence: 99%

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Histamine-Induced Prolactin Release: Pharmacological Characterization of Receptors in Male Rats

Donoso¹,

Zárate²,

Seltzer³

1983

Neuroendocrinology

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“…The stimula tory effect is mediated via activation of HA receptors, but different results have been obtained regarding the specific type of HA receptor (Hi-or H2-receptor) involved. Some investigators reported that the PRL-releasing effect of ICV administered HA to male rats is mediated via H^-receptors, Received: August 7, 1985 Accepted after revision: March 10, 1986 since the response was blocked by H^-receptor antagonists administered ICV but not by H|-receptor antagonists ad ministered ICV or systemically [3,4,19].Other investigators found that HA stimulated PRL se cretion via Hi-receptors and inhibited the secretion via H2-receptors (I, 12, 14, 20]. Thus, in lactating rats the sucklinginduced PRL release was inhibited by ICV and IV adminis tration of Hi-receptor antagonists, whereas the response was not affected by ICV or IV infusion of an Hi-receptor antagonist [1].…”

mentioning

confidence: 99%

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

Knigge¹,

Matzen²,

Warberg³

1986

Neuroendocrinology

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Controversy exists regarding the involvement of H₁- or H₂-receptors in the PRL-releasing activity of histamine (HA). This could be due to differences in the route of administration of HA and histaminergic compounds. Therefore, we studied the effect on PRL secretion of HA and HA-agonists infused intracerebroventricularly (ICV) or systemically (IA) either alone or in combination with HA-antagonists in male rats. HA administered ICV as well as IA stimulated PRL secretion dose dependently. The stimulatory effect of ICV-infused HA was blocked by the H₂-receptor antagonist cimetidine (CIM) and mimicked by the H₂-receptor agonists 4-methylhistamine (4-MeHA) and dimaprit (DIM). In contrast, the H₁-receptor antagonist mepyramine (MEP) enhanced the PRL-releasing effect of HA while the H₁-receptor agonist 2-thiazolylethylamine (2-TEA) had no significant effect. The stimulatory effect of IA-infused HA was blocked by the H₁-receptor antagonist MEP and mimicked by the H₁-receptor agonist 2-TEA, whereas the H₂-receptor antagonist CIM enhanced the PRL-stimulatory effect of HA and the H₂-receptor agonist DIM was without effect. 4-MeHA stimulated PRL secretion, but this effect was unrelated to stimulation of H₂-receptors. The effect of ICV administered HA was unaffected by IA infused antagonists and the effect of IA administered HA was not altered by ICV infused antagonists. HA had no effect on the PRL release from isolated adenohypophyses, and HA did not stimulate PRL secretion in pituitary stalk-sectioned rats following IA infusion. The findings indicate that HA administered ICV exerts its PRL releasing activity via H₂-receptors while HA administered IA stimulates PRL secretion via H₁-receptors. Furthermore, HA administered ICV may inhibit PRL secretion via H₁-receptors and administered IA may inhibit PRL secretion via H₂-receptors. The effect of HA whether infused centrally or systemically is exerted at two discrete suprapituitary sites, presumably within the hypothalamus.

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Histaminergic Transmission in the Brain

Schwartz

Garbarg

Pollard

1986

Comprehensive Physiology

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H<sub>1</sub>- and H<sub>2</sub>-Histamine Receptor Antagonists and Induced Release of Prolactin in Male Rats

Cited by 23 publications

References 6 publications

Histamine-Induced Prolactin Release: Pharmacological Characterization of Receptors in Male Rats

Histamine-Induced Prolactin Release: Pharmacological Characterization of Receptors in Male Rats

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

Histaminergic Transmission in the Brain

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