Effect of Melatonin and 5-Hydroxytryptamine on Aldosterone and Corticosterone Production by Adrenal Glands of Normal and Hypophysectomized Rats

Ea, Gromova; Kraus, Michal; Krecek, J

doi:10.1677/joe.0.0390345

Cited by 38 publications

(8 citation statements)

References 12 publications

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“…This Þnding is supported by reports on the lack of any e¤ect of melatonin on corticosterone production in perfused adrenal glands in vitro (Persengiev et al 1989) and on adrenal growth and cortisol secretion in vivo (Gromova et al 1967;Malendowicz 1985) and humans (Wright et al 1986;Waldhauser et al 1987;Nickelsen et al 1989). Also, the light-induced suppression of nocturnal melatonin secretion had no e¤ect on circulating cortisol in men (McIntyre et al 1992).…”

Section: Discussionmentioning

confidence: 65%

“…Others used isolated pineals or cultured pinealocytes and isolated adrenals or adrenomedullary tissue to study the mutual inßuences of glucocorticoids and melatonin on each others synthesis and release (Giordano et al 1970;Ogle and Kitay 1978;Sanchez de la Pena et al 1983;Touitou et al 1989). It is worth mentioning that the concept of a physiological coupling between glucocorticoid and melatonin secretion has already been questioned by some earlier studies (Gromova et al 1967;DeussenSchmitter et al 1976;Champney et al 1985;Malendowicz 1985;Wright et al 1986;Persengiev et al 1989). Apparently, the more the experimental design chosen by experimentors to explore the putative interactions between both endocrine systems approached reality, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…In some studies, this suppressive action was only observed in females (Dill 1961;Lesniewska et al 1990) or only at certain circadian stages (Sanchez de la Pena et al 1983). Other researchers found no e¤ect of melatonin on adrenal glucocorticosteroid formation and circulating levels of glucocorticosteroids (Gromova et al 1967;Malendowicz 1985;Persengiev et al 1989). Diverging results have also been obtained in human studies.…”

Section: Introductionmentioning

confidence: 93%

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No evidence for a physiological coupling between melatonin and glucocorticoids

et al. 1997

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Much has been speculated about the existence of a physiological coupling between melatonin and glucocorticoid secretion and about a possible anti-stress action of melatonin. We examined the relationship between melatonin and glucocorticoid secretion under close-to-physiological conditions, when the plasma concentration of either melatonin or glucocorticoids was elevated acutely or chronically in both rats and humans. Tryptophan administration caused a massive rise of plasma melatonin, but had no effect on corticosterone levels in rats or on cortisol levels in humans. The acute and long-lasting exposure of rats to uncontrollable stress resulted in a significant rise of adrenal corticosterone secretion, but had no effect on circulating melatonin levels. Orchectomy caused an initial increase in circulating corticosterone (when melatonin was unaffected) and a delayed rise in circulating melatonin (when corticosterone levels were normalized). In humans, no correlation was found between the nocturnal urinary excretion of melatonin and cortisol, either among healthy subjects, or among patients suffering from panic disorder (with an increased urinary excretion of cortisol) or among insomnia patients (with a high incidence of low melatonin secretion). Furthermore, no evidence was found for a suppressive action of melatonin on dexamethasone-mediated thymus regression in rats and on dexamethasone-mediated suppression of lymphocyte proliferation in vitro. Taken together, the results of this study provide no evidence for the existence of mutual influences between melatonin and glucocorticoid secretion, nor do they support the proposed attenuation of glucocorticoid-mediated effects on target cells or tissues by melatonin under physiological conditions.

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

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No evidence for a physiological coupling between melatonin and glucocorticoids

et al. 1997

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“…Pinealectomy has been reported to cause adrenal hypertrophy in rodents [1][2][3][4][5][6] and this effect is neutralized by adminis-tration of pineal extract or melatonin [1,3]. Pinealectomy increases corticosterone secre tion [7][8][9] and disturbs the 24-hour pattern of adrenal activity [6,10], while melatonin treatment has been reported both to increase [10,11] and decrease corticosterone [12][13][14], Pinealectomy also decreases and melatonin administration in vivo in the female rat stimulates 5a-reductase activity in the adre nal gland resulting in an alteration of the proportions of steroids subsequently pro duced by adrenal slices [4,5], Long-term melatonin treatment also causes hypertrophy of the zona glomerulosa and a rise in plasma aldosterone [15],…”

Section: Introductionmentioning

confidence: 99%

Binding Sites for 2-[<sup>125</sup>I]Iodomelatonin in the Adrenal Gland

Brown¹,

Pang²,

Pang³

1994

Neurosignals

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The existence of melatonin receptors in adrenal glands is suggested by effects on rodent adrenal function which follow pinealectomy or in vivo and in vitro melatonin treatment. In 1992, Persengiev and coworkers reported specific binding of 2-[¹²⁵I]iodomelatonin to rat adrenal tissue. In order to study adrenal binding further we have done binding studies on adrenal membranes from ducks sacrificed at midlight. We observed binding of 2-[¹²⁵I]iodomelatonin which was specific, rapid, saturable, stable, reversible and of high affinity. Scatchard plots were linear and Hill coefficients were close to unity supporting the existence of a single class of 2-[¹²⁵I]iodomelatonin binding sites. On Scatchard analysis the K_d was in the physiological range (27.4 pmol/l) together with a B_max of 3.38 fmol/mg protein. Sites were highly specific to melatonin and its two synthetic analogs, 2-iodomelatonin and 6-chloromelatonin in pharmacological studies. In autoradiographic studies on the chicken adrenal gland, one class of 2-[¹²⁵I]iodomelatonin binding site was demonstrated with a K_d of 58.8 pmol/l and B_max of 182 fmol/g tissue. Kinetic and pharmacological studies indicated that these sites are saturable, reversible, and of high specificity and affinity. These findings in the chicken are similar to those of the duck adrenal data obtained by radioreceptor assay. In preliminary studies, no significant difference was found between 2-[¹²⁵I]iodomelatonin binding to the adrenal glands collected at midlight and middark. These high-affinity binding sites are similar to those reported in a wide variety of tissues and are consistent with the hypothesis of direct action of melatonin on the adrenal gland. Further investigations on factors regulating the adrenal 2-[¹²⁵I]iodomelatonin binding sites as well as on the transduction mechanisms of the melatonin-receptor complex in the adrenal gland are essential in order to establish the physiological functions of these sites.

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“…Using the rate at which 1311 disappears from the thyroid as an index, Turner and his associates have concluded that melato nin also slows the secretion of iodinated thyroid hormones (89,(102)(103)(104). Some investigators have observed in vivo decreases in adrenal corticosterone production in rats given large doses of melatonin (50-200 I-'-gliOO g body weight) (105). Others, using smaller doses, have failed to observe changes in either the synthesis of corticosterone or the plasma or pituitary levels of ACTH (1 I-'-g/kg body weight) (106).…”

Section: Other Glandsmentioning

confidence: 99%

The Pharmacology of the Pineal Gland

Minneman¹,

Wurtman²

1976

Annu. Rev. Pharmacol. Toxicol.

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Only recently have a sufficient number of publications been available to legitimize a review of the pharmacology of the mammalian pineal organ. Two decades ago Kitay & Altschule reviewed the world literature on pineal physiology, which comprises several thousand papers, and concluded only that removal of the pineal, or administration of pineal extracts, somehow affected pigmentation in lower vertebrates and gonadal function in mammals (1). As the studies described below demonstrate, much more information is now available concerning the pharmacology of the pineal. This review subdivides present knowledge into two areas: (a) the effects on mammals of administering pineal extracts or pure synthetic or natural pineal constituents and (b) the effects of drugs and hormones on the pineal itself. As might be anticipated, the bulk of studies cited in both categories deals with the pineal hormone, melatonin. Melatonin was first isolated from bovine pineal extracts in 1958 by Lerner and his colleagues (2), who used as a marker the capacity of the hormone to aggregate the pigment granules in amphibian melanophores around the cell nucleus. Five years later, Wurtman et al (3) showed that melatonin affected a physiological function in mammals, that is, the size and secretion of the ovary, and subsequent studies have demonstrated that melatonin administration also modifies the growth, composition, and functional activities of numerous other organs. Only recently an assay was developed that allows quantification of the melatonin in human urine (4). The concentrations of the compound vary with a characteristic daily rhythm, peaking at night. The pineal's apparent role as the sole or major source of melatonin, the presence of melatonin in urine, and the demonstration that physiologic effects follow a pinealectomy or the administration of melatomin seem to justify labeling it a pineal hormone. Melatonin synthesis and pineal biosynthetic activity are generally controlled by the sympathetic nerves of this organ (5,6). Therefore, it should not be surprising that drugs known to modify the synthesis, release, or metabolism of norepinephrine in peripheral organs also affect pineal function. Melatonin is itself a derivative of another biogenic amine, serotonin, whose metabolism and actions are also affected by numerous drugs. Indeed, the pineal has often provided an apt tool for examining monoaminergic mechanisms for pharmacologists not specifically concerned with its particular functional properties.

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Effect of Melatonin and 5-Hydroxytryptamine on Aldosterone and Corticosterone Production by Adrenal Glands of Normal and Hypophysectomized Rats

Cited by 38 publications

References 12 publications

No evidence for a physiological coupling between melatonin and glucocorticoids

No evidence for a physiological coupling between melatonin and glucocorticoids

Binding Sites for 2-[<sup>125</sup>I]Iodomelatonin in the Adrenal Gland

The Pharmacology of the Pineal Gland

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