Influence of histamine and pentobarbitone on plasma and CSF vasopressin levels of hypophysectomized rats

Mens, Wim B.J.; Dam, Anja F. van; Greidanus, T.B. van Wimersma

doi:10.1016/0361-9230(82)90016-8

Cited by 18 publications

(7 citation statements)

References 9 publications

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“…However, in previous studies HA had no effect on the release of bioassayable CRF from hypothalamic tissue in vitro (Fehm et al 1980;Hillhouse et al 1975). AVP may be involved in the mediation of the response to HA, since AVP is released by HA (Dogterom et al 1976;Mens & van Wimersma Greidanus 1982), and since AVP stimulates the release of ACTH and ß-ENDir (Rivier et al 1984;Vermes et al 1980). In summary, HA infused centrally stimulates the release of the POMC-derived peptides ACTH, ß-END, and ß-LPH from the pituitary of male rats.…”

Section: Discussionmentioning

confidence: 93%

Effect of histamine on the secretion of pro-opiomelanocortin derived peptides in rats

Knigge

Bach²,

Matzen³

et al. 1988

Acta Endocrinologica

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In conscious male rats intracerebroventricular infusion of histamine increased the plasma concentrations of ACTH and \g=b\-endorphinimmunoreactivity 2.5-fold (P < 0.01). Gel filtration of plasma revealed two peaks of \g=b\-endorphinimmunoreactivity corresponding to \g=b\-endorphin and \g=b\-lipotropin. The two fractions increased almost equally in histamine-stimulated animals, whereas most of the circulating \g=b\-endorphin immunoreactivity in control animals corresponded to \g=b\-endorphin. Central infusion of the H1\ x=r eq-\ receptor agonist 2-thiazolylethylamine and of the H2\ x=r eq-\ receptor agonists dimaprit or 4-methylhistamine increased the plasma ACTH and \g=b\-endorphin immunoreactivity concentrations 2-and 3-fold, respectively (P < 0.01). Infused intracerebroventricularly, the H2\ x=r eq-\ receptor antagonists cimetidine or ranitidine prevented the histamine-induced increase in plasma ACTH and \g=b\-endorphinimmunoreactivity (P < 0.01), whereas the H1-receptor antagonist mepyramine inhibited the peptide responses by 70% (P < 0.01). Infused intra-arterially cimetidine or ranitidine inhibited the histamine\x=req-\ induced increase in plasma ACTH by 80% (P < 0.01) and plasma \g=b\-endorphinimmunoreactivity by 45% (P < 0.05), whereas mepyramine or the other H1-receptor antagonist SKF-93944 inhibited the ACTH response by 50% (P < 0.05), but had no effect on the \g=b\-endorphinimmunoreactivity. The results indicate that histamine increases the release of the pro-opiomelanocortin derived peptides ACTH, \g=b\-lipotropin and \g=b\-endorphin from the anterior pituitary lobe, whereas an effect of histamine on the release of \g=b\-endorphin from the neurointermediate lobe is possible. The effect of histamine seems primarily mediated by H2-receptors, whereas H 1-receptors appear to play a minor role.

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Section: Discussionmentioning

confidence: 93%

Effect of histamine on the secretion of pro-opiomelanocortin derived peptides in rats

Knigge

Bach²,

Matzen³

et al. 1988

Acta Endocrinologica

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“…This occurs in an environment in which astrocytes are lacking. In fact, after 30 days neu rosecretory neurons have recovered functionally to the ex tent that circulating levels of vasopressin are indistinguish able from those in intact controls [22][23][24]. When severance occurs within the hypothalamus, however, axon regenera tion is limited by astrocytic glial scar formation (unpu blished observations).…”

mentioning

confidence: 91%

“…When transected at the level of the median eminence or the hypophysial stalk, ax onal growth cones develop and establish new neurohemal contacts with the primary capillary plexus of the hypophy sial portal system which, together with pituicyte prolifera tion, eventually leads to the formation of a miniature neural lobe-like structure [13,20, 29, 30, 32]. Concurrent with this morphologic recovery is the reestablishment of near normal levels of hormone secretion and water balance [22][23][24]. When transected within the hypothalamus, however, neu rosecretory axons either do not regenerate [26] or they only regenerate to a rather limited extent [19] without concomi tant functional recovery.…”

mentioning

confidence: 99%

Peptidergic Neurosecretory Axons Regenerate into Sciatic Nerve Autografts in the Rat Hypothalamus

Hd¹,

Lf²,

Bellin³

1986

Neuroendocrinology

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Pieces of intact or degenerated sciatic nerves autografted into contact with transected neurosecretory axons within the hypothalamus were invaded by neurophysin-positive axons. With increasing time after grafting, increasing numbers of axons were present in both types of grafts, but grafts of degenerated sciatic nerves always contained more axons. At the fine-structural level typical neurosecretory as well as nonneurosecretory axons were usually associated with basal lamina-enclosed neurolemmocyte processes; occasional axons occurred among collagen fibrils or within basal lamina scaffolds. Profiles with the fine structural characteristics of axon terminals were present by 20 days after transplantation.

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“…Among its most conclusive actions are the neuromodulation of the corticotropinergic system [7] and a potent activity as vaso pressin (VP) releaser [11,[26][27][28]44]. The administration of HA, centrally or peripherally, reduces the urine output.…”

Section: Introductionmentioning

confidence: 99%

Histaminergic Neuromodulation of the Release of Vasopressin

et al. 1987

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In an attempt to clarify the nature of histaminergic neuromodulation of the vasopressinergic system, several studies under different experimental paradigms were carried out. L-Histidine loads (8 mmol/kg, i.p.) induced a marked increase in histamine (HA) in the anterior (AHR) and posterior (PHR) hypothalamic regions, the median eminence (ME) and adenohypophysis (Ah) with no apparent effect on the concentration of HA in the neurohypophysis (Nh), as measured by high-performance liquid chromatography. These findings correlated with decreases in vasopressin (VP) levels in the AHR and ME, accompanied by increases of the neuropeptide in the PHR and Ah. Intraperitoneal injections of HA (6 µmol/kg), resulted in a significant (p < 0.005) rise in VP levels in the PHR, ME and Ah. HA induced an elevation of VP in the prefrontal cortex (PFC) from 6.23 ± 2.02 to 43 ± 4.05 µU/mg, as well as a 60% reduction in neurohypophyseal VP. These HA-induced VP responses were abolished by both mepyramine (3 µmol/kg) and famotidine (4 µmol/kg) in the PHR and PFC. Mepyramine suppressed the HA-induced VP response in the Ah and enhanced it in the Nh, while famotidine did the opposite. When alpha-fluoromethylhistidine (FMH), an irreversible inhibitor of histidine decarboxylase, was administered at doses of 100 mg/kg/day (i.p.), hypothalamic HA levels fell by 40–45% after 1 h, by 50% after 3 h, and by 65–80% after 24 h in adrenalectomized rats. In the same conditions, but after a week of treatment with FMH, the VP response to adrenalectomy was clearly impaired. These results seem to demonstrate that the physiological levels of neuronal HA are indispensable for the normal functioning of the neuroendocrine system. In this context, preliminary pharmacological evidence showed that histaminergic neuromodulation of the vasopressinergic system is mediated through H₁ receptors in the Ah, H₁ receptors in the ME and Nh, and both H₁ and H₂ receptors in the PFC and hypothalamus.

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Influence of histamine and pentobarbitone on plasma and CSF vasopressin levels of hypophysectomized rats

Cited by 18 publications

References 9 publications

Effect of histamine on the secretion of pro-opiomelanocortin derived peptides in rats

Effect of histamine on the secretion of pro-opiomelanocortin derived peptides in rats

Peptidergic Neurosecretory Axons Regenerate into Sciatic Nerve Autografts in the Rat Hypothalamus

Histaminergic Neuromodulation of the Release of Vasopressin

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