Elevation of Serum Corticosterone Concentrations in Rats by Pergolide and Other Dopamine Agonists

The Blunted Plasma Cortisol Response to Apomorphine and Its Relationship to Treatment Response in Patients with Schizophrenia

“…In addition, the pergolide-stimulated corticosterone response was blocked by centrally acting antagonists (e.g. haloperidol and spiperone) but not by a peripherally acting DA antagonist (domperidone) (Fuller and Snoddy 1981). Administration of a D 1 or D 2 agonist, or the DA uptake inhibitor GBR 12909 into the third ventricle or the paraventricular nucleus of the hypothalamus (but not into the lateral ventricle), stimulated the HPA axis Kuhn 1992, 1993).…”

Bromocriptine-Induced Hyperglycemia in Nonobese Diabetic Mice: Kinetics and Mechanisms of Action

“…Regardless of their origin, catecholamines inhibit insulin secretion through specific α2-adrenergic receptors present on β-cells [29]. Still at the β-cell level, corticosteroids, the secretion of which is strongly enhanced by bromocriptine (present data and [14,15]), might potentially be responsible for part of the inhibitory effect observed, because of the presence of specific glucocorticoid receptors in β-cells and their rapid inhibitory effect on pancreatic insulin release [30][31][32][33]. Corticosteroids may also have more long-term inhibitory effects on insulin synthesis.…”

“…The D2-dopaminergic antagonist, metoclopramide, completely inhibits late bromocriptine effects on NOD corticosterone levels, suggesting an action mediated by specific D2-dopaminergic-receptor stimulation. In rats, the observation that the pergolideinduced increase in corticosterone is blocked by haloperidol, a dopaminergic antagonist that acts both centrally and peripherally, but not by the peripheral antagonist, domperidone, is indicative of central D2-dopaminergic-receptor involvement [15]. These receptors are probably located in the hypothalamus, since direct quinpirole administration into the third ventricle increases serum adrenocorticotrophic hormone (ACTH) levels in rats [13].…”

“…With regard to catecholamines, the stimulatory effect of the D2-dopaminergic agonist, quinpirol, on epinephrine release from rat adrenals [12], strongly suggests that they are involved in inducing hyperglycemia. Finally, measurement of circulating glucocorticoids has been used routinely in rats to evaluate D2-dopaminergic activity and dose-dependent increases in serum corticosterone following the injection of various D2-dopaminergic agonists [13][14][15].…”

Evidence of the dopamine-2 receptor mediated inhibition of the hypothalamic-pituitary-adrenal system; a rodent model of hypercortisolism in chronic neuropsychiatric disorders

“…However, to our surprise, haloperidol at higher doses even augmented the ether evoked corticosterone response. Because the available literature reflects conflicting data regarding the action of antipsychotics on the HPA axis [23,30,40], in separate, dose-response experiments, the intrinsic activity of D 2 antagonism on the HPA system was investigated. It was not only the inconsistent literature but the increasingly recognized importance of the CRH positive neural networks in the development of dopaminergic system-related disorders [23,35,[41][42][43][44][45] that motivated us to investigate this question.…”