Adrenal Gland Rhythmicity and Pituitary Regulation of Adrenal Steroid Secretion

Mann, David R.; Cost, Michael G.; Jacobson, Carol D.; Macfarland, Leslie A.

doi:10.3181/00379727-156-39953

Cited by 16 publications

(13 citation statements)

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“…They proposed that prolac tin diminished 5a-reductasc activity in corti cal cells, thus decreasing intra-adrenal degra dation of corticosterone, but that overall ste roidogenesis was not enhanced. Our in vitro data, as well as the in vivo results of Mann et al [4], clearly show that, in addition to long term effects on intra-adrenal metabolism, prolactin can also transiently influence secre tory activity of a variety of adrenal steroids. The acute potentiating actions of prolactin observed by ourselves, and Mann et al [4], implies that prolactin may shift adrenal en zyme activity for steroidogenesis as well as for metabolism, and in all three anatomical zones of the cortex.…”

Section: Discussionsupporting

confidence: 50%

“…Mann et al [4] induced in vivo release of progesterone and corticosterone with intra venous injections of prolactin to rats. Studies by Parker et al [16], however, failed to show any such stimulation in sheep or dogs.…”

Section: Discussionmentioning

confidence: 99%

“…There is convincing evi dence that cortical cells contain specific re ceptors for the hormone [1][2][3]. Administra tion of prolactin to rats stimulated corticoste rone [4] and progesterone [4. 5] output in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Prolactin Stimulates and Potentiates Adrenal Steroid Secretion in vitro

Eldridge¹,

Lymangrover²

1984

Horm Res

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Prolactin, alone and in combination with ACTH, was tested for its ability to release steroids from rat adrenocortical slices superfused in vitro. The hormone possessed weak activity alone (minimal responsive dose = 1 U), but was able to potentiate the ACTH-stimulated corticoid release at much lower doses (significant response over ACTH alone at 0.01 U prolactin). This latter dosage was calculated to be within the physiologic range of prolactin in blood. Analysis of individual steroids in superfusate by RIA revealed that aldosterone release was most sensitive to prolactin, followed by corticosterone, androstenedione, and progesterone. We conclude that prolactin is an adrenocortical secretagogue of physiological relevance in the rat, and that it could play a role in enhancing the action of ACTH to acutely release steroids.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

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Prolactin Stimulates and Potentiates Adrenal Steroid Secretion in vitro

Eldridge¹,

Lymangrover²

1984

Horm Res

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“…There do not appear to be any reports of prolactin directly affecting ACTH or CRF secretion, however, in vitro studies of the adrenal cortex have shown that prolactin can enhance ACTH-induced corticosterone secretion, without affecting basal corticosterone secretion [6]. Furthermore, injections of prolactin have been shown to attenuate dexamethasoneinduced suppression of corticosterone levels [15]. Based on these observations, a decrease in prolactin levels by cys teamine would be expected to decrease corticosterone se cretion.…”

Section: Discussionmentioning

confidence: 99%

Effects of Systemic and Intracerebroventricular Cysteamine on Dexamethasone-Induced Suppression of Corticosterone Levels in the Rat

Radke

Vincent²

1988

Neuroendocrinology

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To investigate whether somatostatin systems plays a significant role in the regulation of the hypothalamic-pituitary-adrenal axis, the effects of cysteamine, a drug which reduces somatostatin levels, on the dexamethasone-induced suppression of plasma corticosterone levels were examined in the rat. Male Long Evans rats were handled daily for 1 week prior to receiving a standard dexamethasone suppression test. On the 1st day, rats received a 9.00 a.m. saline injection and blood samples were taken from the tail at 1.00 p.m. On the 2nd day, rats received dexamethasone or saline at 9.00 a.m. and a second blood sample was taken at 1.00 p.m. Experimental groups were pretreated with systemic injections of cysteamine, 5 min or 14 h, prior to receiving dexamethasone. Additional groups, previously implanted with guide cannulae, were given an infusion of cysteamine or saline into the lateral ventricle 14 h prior to dexamethasone. Circulating corticosterone levels were determined by radioimmunoassay. Rats were sacrificed immediately following each experiment and the hypothalamus dissected and assayed for levels of somatostatin immunoreactivity. The results of the first experiment showed that dexamethasone (10 µg/kg) alone reduced plasma corticosterone levels from control values (174 + 36 ng/ml) to undetectable levels ( < 25 ng/ml). Pretreatment with cysteamine 5 min prior to dexamethasone, while having no significant effect on basal corticosterone levels, completely blocked the dexamethasone-induced suppression of corticosterone levels. Similar observations were obtained with rats pretreated with cysteamine 14 h prior to dexamethasone. In contrast, intracerebroventricular cysteamine pretreatment did not block the dexamethasone-induced suppression of corticosterone levels. These results add further evidence in support of an involvement of somatostatin systems in the regulation of the hypothalamic-pituitary-adrenal axis.

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“…Plasma B concentrations were elevated 1 h after the last B injection to levels which were threefold HOURS AFTER CORTICOSTERONE ADMINISTRATION greater than preinjection values. These values returned to basal levels within 12 h. Changes in plasma B following the last B injection closely mimicked the normal B rhythm ob served in intact animals from our colony [19]. No signifi cant fluctuations in B were observed in vehicle-injected ani mals.…”

Section: Resultsmentioning

confidence: 68%

Influence of Corticosterone on the Response to Gonadotropin-Releasing Hormone in Rats

Ir¹,

Mann²

1981

Neuroendocrinology

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The objective of this study was to determine whether the diurnal rhythm of corticosterone (B) alters the response of the pituitary to gonadotropin-releasing hormone (GnRH). Mature female rats housed in constant illumination were ovariectomized (Ovx) and adrenalectomized (Adx), and maintained on either corticosterone (B, 160 μg/ml in drinking water) or 0.9% saline. 3 weeks later a silastic implant of estradiol (E2) was implanted subcutaneously into each animal. For the next 5 days B-maintained rats received a daily injection of either B (250 μg/100 g BW) or vehicle at 05.00 or 17.00 h. Groups of rats were sacrificed at 0, 1, 3, 6, 12 and 18 h after the fifth injection, and plasma B and E2 were measured. Other animals were challenged with GnRH (1.0 ng/100 g BW) at 0, 6, 12 and 18 h after the last B injection. The fifth B injection initiated changes in plasma B which closely mimicked the normal B rhythm in intact rats. E2 levels (approximately 100 pg/ml) remained fairly constant over the same period. In rats receiving B injection at 17.00 h, the response to GnRH was altered by B administration. The LH response was greatest 6 h after B was injected, and animals showed a lower response at other times. The same relationship between circulating B and the response to GnRH could not be demonstrated in rats injected with B at 05.00 h. Animals maintained on saline exhibited higher basal LH levels, a longer mean half-life of LH, and the plasma LH response to GnRH was lower than in animals receiving B therapy. These results indicated that: (1) physiological dosages of B can alter the response to GnRH in constant light rats; (2) B has a potentiating effect on this response, and (3) B may also influence the clearance rate for LH.

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Adrenal Gland Rhythmicity and Pituitary Regulation of Adrenal Steroid Secretion

Cited by 16 publications

References 0 publications

Prolactin Stimulates and Potentiates Adrenal Steroid Secretion in vitro

Prolactin Stimulates and Potentiates Adrenal Steroid Secretion in vitro

Effects of Systemic and Intracerebroventricular Cysteamine on Dexamethasone-Induced Suppression of Corticosterone Levels in the Rat

Influence of Corticosterone on the Response to Gonadotropin-Releasing Hormone in Rats

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