Effect of Dopamine on ACTH-Induced Glucocorticoid Secretion in Rat Adrenal Suspended Cells

Matsuki, Michihiro; Nishida, Seikoh; Kashiwa, Yasuhiro; Horino, Masaharu; Yoneda, Masashi; Endoh, Masahiko; Satoh, Atsuko; Oyama, Hideki

doi:10.1055/s-2007-1013567

Cited by 10 publications

(6 citation statements)

References 4 publications

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“…This decrease occurs at a time when the diurnal rhythm of plasma cortisol concentrations in pigs are decreasing from their maximal levels (24), which may suggest that reductions of PRL alter this diurnal rhythm. However, the current results provide only modest support for the hypothesis that PRL, or dopamine (30,31), modulates porcine adrenocortical function. Similarly, conclusive effects of CB154 and associated reductions in plasma PRL on the aspects of lymphocyte activity measured were absent.…”

Section: Discussioncontrasting

confidence: 88%

Pituitary-Adrenocortical and Lymphocyte Responses to Bromocriptine-induced Hypoprolactinemia, Adrenocorticotropic Hormone, and Restraint in Swine

Klemcke

Blecha

Nienaber

1990

Experimental Biology and Medicine

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A study was conducted with castrated male pigs (barrows) to evaluate effects of bromocriptine-induced hypoprolactinemia (6 days) on basal and adrenocorticotropic hormone (ACTH)-altered (single injection) pituitary-adrenocortical function, on lymphocyte proliferative responses, and on interleukin 2 production. In addition, the study was designed to measure the short time course of pituitary-adrenocortical and lymphocyte responses to ACTH and to a 30-min restraint stressor. Blood samples were taken via indwelling jugular catheters at -0.5, +0.5, +2, and +5 hr (with reference to time of acute treatment exposure) on Day 6 of the study. Lymphocyte responses were measured only at the 2-hr interval. Exposure (6 days) to bromocriptine (CB154) was associated with 53% reductions (P less than 0.05) in plasma prolactin (1.37 +/- 0.13 vs 0.60 +/- 0.04 vs 0.68 +/- 0.08 ng/ml) when averaged across all time intervals in control, CB154-treated, and CB154 + ACTH-treated pigs, respectively. The reductions in plasma prolactin were associated with a reduction (P less than 0.05) in basal plasma cortisol at only one time interval (+0.5 hr) when CB154-treated pigs were compared with controls (17.7 +/- 4.2 vs 26.9 +/- 3.2 ng/ml). CB154 had no effect on plasma ACTH or growth hormone concentrations for the time periods at which they were measured. CB154 treatment produced numerical, but not statistically significant, 38% reductions in interleukin 2 production (6.31 +/- 1.8 vs 3.91 +/- 1.47 units/ml). Lymphocyte proliferative responses to the mitogen concanavalin A and interleukin 2 production decreased 65 and 75% (P less than 0.05), respectively, 2 hr subsequent to ACTH administration when compared with control animals. Hence, under the conditions of this study, only a modest association between lowered plasma prolactin concentrations and basal cortisol concentrations was evident. The data suggest the absence of dopamine regulation of basal plasma ACTH in pigs and provide evidence for a rapidly occurring inhibitory effect of ACTH administration on specific lymphocyte activities.

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Section: Discussioncontrasting

confidence: 88%

Pituitary-Adrenocortical and Lymphocyte Responses to Bromocriptine-induced Hypoprolactinemia, Adrenocorticotropic Hormone, and Restraint in Swine

Klemcke

Blecha

Nienaber

1990

Experimental Biology and Medicine

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“…Numerous experiments have suggested that aldosterone secretion from the zona glomerulosa is under tonic dopaminergic inhibitory control [35][36][37][38][39]. However, effects of dopamine on secretion from the zona fasciculata have been equivocal [40,41 ]. A variety of neuropeptides have been identified in nerve endings within the adrenal cortex and medulla and in medullary chromaffin cells [42], Functional studies have shown that vasoactive intestinal peptide (VIP) sti mulates the release of corticosteroids from the zona glomerulosa [43] and the zona fascieulata [44][45][46].…”

Section: Discussionmentioning

confidence: 99%

Splanchnic Nerve Stimulation Modulates Steroid Secretion in Hypophysectomized Dogs

Engeland

Gann²

1989

Neuroendocrinology

101

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To test whether or not splanchnic neural input to the adrenal gland affects secretion of steroids from the adrenal cortex, the thoracic splanchnic nerve was electrically stimulated in pentobarbital-anesthetized dogs after hypophysectomy and replacement with physiological concentrations of ACTH. An adrenal vein cannula was placed to permit measurement of cortisol, corticosterone, 11 -deoxycortisol, epinephrine and norepinephrine secretion rates and adrenal blood flow. Plasma ACTH was measured and the presentation rate of ACTH was calculated as the product of plasma ACTH concentration and adrenal plasma flow. Dogs were infused initially with ACTH for 60 min at 2 ng/min followed by infusion for 60 min at 10 ng/min. Within each infusion period, the distal end of the nerve was stimulated (20 V; 0.5-ms pulse duration) at 4 and at 20 Hz for 10 min each. Nerve stimulation resulted in a frequency-dependent increase in mean arterial pressure, in epinephrine and norepinephrine secretion and in adrenal blood flow. Arterial ACTH remained constant during nerve stimulation; however, increased adrenal blood flow resulted in increased presentation rate of ACTH to the adrenal. Cortisol secretion increased in response to nerve stimulation at 4 and 20 Hz during infusion of 2 and 10 ng/min ACTH and occurred prior to changes in presentation rate of ACTH. Corticosterone secretion also increased after stimulation at both frequencies, but the response was observed only during infusion of 10 ng/min ACTH. In contrast, 11-deoxycortisol decreased after nerve stimulation at 4 Hz but showed no response after stimulation at 20 Hz during infusion of 2 and 10 ng/min ACTH. Steroid ratios were calculated to assess the possible involvement of specific steroidogenic enzymes in the observed responses. The cortisol to 11-deoxycortisol ratio was increased, whereas the cortisol to corticosterone ratio was not affected by nerve stimulation, suggesting a change in 11-β-hydroxylase activity. These data show that splanchnic nerve stimulation can increase cortisol secretion independently of changes in arterial ACTH. The effect of splanchnic nerve activity on cortisol secretion may result from increasing vascular delivery of ACTH to the adrenal, from release of a non pituitary humoral factor with steroidogenic activity or from direct stimulation of steroidogenesis by an adrenal neurotransmitter substance.

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“…Preferential expression of D2 receptors is observed in the zona glomerulosa (aldosterone secretion) as compared to the zona fasciculata (glucocorticoid secretion), in accordance with an inhibitory role of dopamine and D2 receptors on aldosterone secretion (Pivonello et al 2007). However, a direct inhibitory role of dopamine through D2 receptors on glucocorticoid secretion in the rat zona fasciculata rat is possible, despite controversial results (Matsuki et al 1985;Goebel et al 1992;Kan et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Dopamine D1 and D2 dopamine receptors regulate immobilization stress-induced activation of the hypothalamus-pituitary-adrenal axis

Belda

Armario

2009

Psychopharmacology

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Dopamine, acting through both D1 and D2 receptors, exerts a stimulatory role on the activation of the HPA axis in response to a severe stressor. The finding that dopamine is involved in the maintenance of post-stress activation of the HPA axis is potentially important because the actual pathological impact of HPA activation is likely to be related to the area under the curve of plasma glucocorticoid levels, which is critically dependent on how long after stress high levels of glucocorticoid are maintained.

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Effect of Dopamine on ACTH-Induced Glucocorticoid Secretion in Rat Adrenal Suspended Cells

Cited by 10 publications

References 4 publications

Pituitary-Adrenocortical and Lymphocyte Responses to Bromocriptine-induced Hypoprolactinemia, Adrenocorticotropic Hormone, and Restraint in Swine

Pituitary-Adrenocortical and Lymphocyte Responses to Bromocriptine-induced Hypoprolactinemia, Adrenocorticotropic Hormone, and Restraint in Swine

Splanchnic Nerve Stimulation Modulates Steroid Secretion in Hypophysectomized Dogs

Dopamine D1 and D2 dopamine receptors regulate immobilization stress-induced activation of the hypothalamus-pituitary-adrenal axis

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