Psychopharmacological Effects and Pituitary—Adrenal Activity

Marks, Bernard H.; Hall, M. M.; Bhattacharya, A.N.

doi:10.1016/s0079-6123(08)61519-8

Cited by 20 publications

(10 citation statements)

References 16 publications

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“…Differences in species studied, in experimental design and in the type of drugs used might account for these discrepancies. On the other hand, there are data by other workers, obtained in experimental animals, which fully agree with ours (2,(11)(12)(13)(14).…”

Section: Discussionsupporting

confidence: 93%

“…In fact, while the importance of this monoamine for the maintenance of the circadian rhythm of ACTH secretion is adequately documented (1,2,9,10), little is known about its possible involvement in the ACTH secretion in response to either physiological or pharmacological provocative stimuli. In this connection, data derived from the experimental animal have shown either a stimulating (2,(11)(12)(13)(14) or an inhibiting (15)(16)(17)(18)(19)(20)(21)(22) effect of serotonin on ACTH secretion, whereas insufficient studies on humans have been performed to obtain reliable data. One recent study, however, has shown an increase in plasma ACTH levels following oral administration of 5-HTP in man (3).…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of ACTH Response to Oral and Intravenous Metyrapone by Antiserotoninergic Treatment in Man

Cavagnini

Panerai

Valentini

et al. 1975

The Journal of Clinical Endocrinology & Metabolism

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Plasma ACTH levels after oral and iv metyrapone administration were studied in 7 and 5 healthy women respectively both under basal conditions and after a 4-day treatment with metergoline, a specific antiserotoninergic agent. In 3 additional women, the effects of methysergide, another antiserotoninergic drug, on the plasma ACTH rise induced by oral metyrapone, were evaluated. A significant lowering of the plasma ACTH levels attained after either oral or iv metyrapone was observed following metergoline administration: 149+/-64.3 vs 239+/-49.1 pg/ml (mean peak values), P less than 0.05 in the oral test and 331+/-19.7 vs 221+/-19.5 pg/ml, P less than 0.02 in the iv test. The fall of plasma cortisol caused by metyrapone was comparable before and after the antiserotoninergic treatment. An interference of metergoline in the ACTH radioimmunoassay was also excluded. After metergoline administration, a slight reduction in the baseline plasma ACTH values was noted: 79+/-7.7 vs 67+/-7.7 pg/ml (NS). A decrease, however not statistically significant, of the metyrapone-induced plasma ACTH elevation occured after methysergide administration: 421+/-150.7 vs 344+/-135.1 pg/ml. These results can be interpreted as indicating that antiserotoninergic treatment caused an inhibition of hypophysial ACTH release in response to metyrapone. Caution is recommended, however, before concluding, on the basis of these findings, that serotonin as such plays a physiological stimulating role on ACTH secretion.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Inhibition of ACTH Response to Oral and Intravenous Metyrapone by Antiserotoninergic Treatment in Man

Cavagnini

Panerai

Valentini

et al. 1975

The Journal of Clinical Endocrinology & Metabolism

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“…This idea is supported by the finding that DB implanted in the MAR did not alter the adrenal weight, except for an increase in adrenal weight in the short-term experiment which may be ascribable to stress resulting from the surgical operation. The hypotheses that NE in ME is not involved in the regulation of CRF is in agreement with the finding that depletion of mono amines in the rat basal hypothalamus by implanting reserpine close to the ME failed to modify the pituitary-adrenal response to various stressful stimuli [33], However, the intraventricular administration of DA and NE inhibited the release of ACTH in the reserpine-pretreated rat [24] and in the dog [36]. In these experiments, there is the possibility that DA and NE might have affected a region outside of ME.…”

Section: Discussionsupporting

confidence: 87%

Effects of Norepinephrine and Dibenamine Implanted in the Median Eminence on the Estrous Cycle of the Rat

Uemura¹,

Kobayashi²

1974

Horm Res

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A cannula containing a mixture of norepinephrine (NE) or dibenamine (DB) and cholesterol (C) was implanted into different hypothalamic regions or adenohypophysis of rats. The rats bearing implants of NE in the median eminence-arcuate nucleus region (MAR) showed irregular estrous cycles or prolonged diestrus and their ovaries had few follicles and atrophic corpora lutea. Thus, NE suppressed the secretion of FSH and LH at the level of the median eminence. The rats implanted with DB in MAR had prolonged diestrus, and their uteri showed decidual reaction, indicating that an α-adrenergic mechanism is involved in the release of PTF from the median eminence.

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“…Clonidine, an a-adrenergic drug, also inhibits the stressinduced ACTH secretion in anesthetized dogs [9]. The catecholamine-mediated inhi bition of ACTH secretion is more difficult to demonstrate in species other than the dog [2, 18,22], In rats a number of arguments have been gathered in favor of the inhibitory role of central catecholamine pathways, but also an excitatory role has been postulated [16,30], In in vitro studies in which the isolated rat hypothalamus is used, noradrenaline in hibits the release of a corticotrophin-releasing factor [ 1,15], The depletion of brain nor adrenaline by a-methyl-p-tyrosine (a-MT) [23,24] or by reserpine [7,21] leads to a hypersecretion of ACTH, but an intraperitoneal (i.p.) injection of clonidine has no effect on plasma corticosterone levels in rats [14,27],…”

Section: Introductionmentioning

confidence: 99%

Effect of Intracerebroventricular Clonidine on Serum Corticosterone Levels in Rats

Zacny¹,

Bugajski²

1984

Horm Res

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In conscious, nonstressed rats clonidine given intracerebroventricularly (i.c.v.) increased the pituitary-adrenocortical response evaluated indirectly from corticosterone concentration. The maximum significant increase occurred 60 min after a dose of 10 µg. The α₂-adrenoceptor antagonist yohimbine given alone i.c.v. in low doses (0.05–1 µg) had no effect on plasma corticosterone levels, but at higher doses (5 and 10 µg) it produced a significant rise in these levels. Phenoxybenzamine (0.05-10 µg, i.c.v.) caused a dose-related increase in corticosterone secretion. Pretreatment of rats with yohimbine considerably antagonized (up to 70%) the increase of corticosterone response induced by clonidine. Phenoxybenzamine failed to alter this effect. The depletion of brain catecholamines by α-methyl-p-tyrosine caused an increase in serum corticosterone concentration. The rise was suppressed by clonidine (10 µg, i.c.v.), and this suppression was antagonized in part by pretreatment with yohimbine. These data support the concept of the noradrenergic inhibition of ACTH secretion in rats. It seems likely that clonidine injected i.c.v. induces stimulation of corticosterone through the activation of presynaptic α₂-adrenoceptors and inhibition of noradrenaline release. The clonidine induced inhibition of corticosterone after α-methyl-p-tyrosine seems to be mediated by α-adrenoceptors located postsynaptically.

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Psychopharmacological Effects and Pituitary—Adrenal Activity

Cited by 20 publications

References 16 publications

Inhibition of ACTH Response to Oral and Intravenous Metyrapone by Antiserotoninergic Treatment in Man

Inhibition of ACTH Response to Oral and Intravenous Metyrapone by Antiserotoninergic Treatment in Man

Effects of Norepinephrine and Dibenamine Implanted in the Median Eminence on the Estrous Cycle of the Rat

Effect of Intracerebroventricular Clonidine on Serum Corticosterone Levels in Rats

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