Bromocriptine inhibits norepinephrine release

Ziegler, Michael G.; Lake, C. Raymond; Williams, Ann C.; Teychenne, Paul F.; Shoulson, Ira; Steinsland, Odd S.

doi:10.1002/cpt1979252137

Cited by 84 publications

(22 citation statements)

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“…However, bromocriptine has not been shown to have any effects on neurotransmitter reuptake or monoamine oxidase [59]. The marked decrease in the metabolites of NE and 5-HT that we found correlates with the reduced NE release after chronic bromocriptine treatment shown by others [60, 61], and offers strong evidence of reduced activities in the noradrenergic and serotonergic neurons after chronic bromocriptine treatment. A very likely explanation for the reduced NE and 5-HT neuronal activities induced by bromocriptine may be its stimulation of presynaptic adrenergic α 2 and 5-HT 1A receptors [62] which therefore inhibited the synthesis, release and subsequent metabolite production of norepinephrine and serotonin, respectively.…”

Section: Discussionsupporting

confidence: 58%

“…Furthermore, direct interaction of bromocriptine with dopaminergic receptors can reduce NE and 5-HT neuronal activities [63]. It has been shown that somatodendritic and synaptic terminal D 2 activation reduces synaptic noradrenaline release [61] and somatodendritic D 2 receptor activation in the raphe reduces terminal serotonin release [64]. Reduction in HVA levels after bromocriptine has been reported numerous times [65, 66] and is consistent with an action of a receptor agonist, which may be due to either a negative feedback mechanism of activation of the postsynaptic receptor [67] or presynaptic D 2 receptor activation [62], leading to decreased dopamine release.…”

Section: Discussionmentioning

confidence: 99%

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Bromocriptine Reduces Obesity, Glucose Intolerance and Extracellular Monoamine Metabolite Levels in the Ventromedial Hypothalamus of Syrian Hamsters

1998

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We examined whether reductions in body fat stores and insulin resistance in Syrian hamsters induced by bromocriptine are associated with reductions in daily norepinephrine (NE) and serotonin activities as indicated by their extracellular metabolite levels in the ventromedial hypothalamus (VMH). High levels of these monoamines within the VMH have been suspected to induce obesity and insulin resistance. Microdialysate samples from the VMH of freely moving obese male hamsters (BW: 208 ± 5 g) were collected hourly over a 25-hour period before bromocriptine treatment, during the first day of and after 2 weeks of bromocriptine treatment (800 µg/animal daily, i.p.), and body composition and glucose tolerance analyses were conducted before and after 2 weeks of treatments. The microdialysate samples were analyzed by HPLC for metabolites of serotonin: 5-hydroxy-indoleacetic acid (5-HIAA), NE: 3-methoxy-4-hydroxy-phenylglycol (MHPG), and dopamine: homovanillic acid (HVA). Bromocriptine treatment for 14 days significantly reduced body fat by 60% and areas under the glucose and insulin curves during a glucose tolerance test by 50 and 46%, respectively. Concurrently, extracellular VMH contents of 5-HIAA, MHPG, and HVA were reduced by 50, 29 and 66%, respectively (p < 0.05). Similarly, VMH 5-HIAA and MHPG contents were 48 and 44% less, respectively (p < 0.05), in naturally glucose-tolerant hamsters compared with naturally glucose-intolerant hamsters. Bromocriptine induced reductions of body fat, and improvements in glucose intolerance may result in part from its ability to decrease serotonin and NE activities in the VMH.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Bromocriptine Reduces Obesity, Glucose Intolerance and Extracellular Monoamine Metabolite Levels in the Ventromedial Hypothalamus of Syrian Hamsters

1998

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“…Furthermore, bromocriptine may be acting centrally to reduce elevated sympathetic tone [48, 49], which can contribute to the pathophysiology of obesity and diabetes in part by potentiating insulin resistance [50, 51, 52]. Bromocriptine may also influence metabolism by modulating hypothalamic centers regulating the pituitary-adrenal axis such as the suprachiasmatic nuclei and/or paraventricular nuclei.…”

Section: Discussionmentioning

confidence: 99%

Intracerebroventricular Administration of Bromocriptine Ameliorates the Insulin-Resistant/Glucose-Intolerant State in Hamsters

Luo

Liang

Cincotta³

1999

Neuroendocrinology

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Bromocriptine, a potent dopamine D₂ receptor agonist, suppresses lipogenesis and improves glucose intolerance and insulin resistance. Recent evidence suggests that bromocriptine may produce these effects by altering central nervous system (CNS) regulation of metabolism. To determine whether or not the CNS plays a critical role in these bromocriptine-mediated effects on peripheral metabolism, we compared the metabolic responses to bromocriptine when administered peripherally versus centrally in naturally obese and glucose intolerant Syrian hamsters. Male hamsters (BW 194 ± 5 g) were treated with bromocriptine or vehicle either intraperitoneally (i.p., 800 µg/animal) or intracerebroventricularly (i.c.v., 1 µg/animal) daily at 1 h after light onset for 14 days while held on 14-hour daily photoperiods. Glucose tolerance tests (GTTs, 3 g glucose/kg BW) were conducted after treatment. Compared to control animals, bromocriptine i.p. significantly reduced weight gain (11.7 vs. –2.4 g) and the areas under the glucose and insulin GTT curves by 29 and 48%, respectively. Similarly, compared with vehicle-treated controls, bromocriptine i.c.v. at 1 µg/animal substantially reduced weight gain (8.7 vs. –6.3 g), the areas under the glucose and insulin GTT curves by 31 and 44% respectively, and the basal plasma insulin concentration by 41% (p < 0.05). Furthermore, both treatments significantly improved insulin-mediated suppression of hepatic glucose production during a hyperinsulinemic-euglycemic clamp. Thus, daily administration of bromocriptine at a very low dose i.c.v. replicates the metabolic effects of bromocriptine administered i.p. at a much higher dose. This finding demonstrates for the first time that the CNS is a critical target of bromocriptine’s metabolic effects.

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“…3 Clinical studies show a DAergic modulation of sympathetic activity in hypertensive and obese individuals, 4 and DAergic agonists have been successfully used as a treatment for hypertension by reducing adrenergic neurotransmission at sympathetic endings. 5 As bromocriptine treatment in obese humans elicited a reduction of serum leptin values 6 and improved insulin sensitivity, 7 this indirectly suggests beneficial effects of reduced DAergic activity.…”

Section: Introductionmentioning

confidence: 99%

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

Álvarez-Aguilar¹,

Alvarez-Paredes²,

Lindholm³

et al. 2013

IJNRD

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Background A reduction of dopaminergic (DAergic) activity with increased prolactin levels has been found in obese and hypertensive patients, suggesting its involvement as a pathophysiological mechanism promoting hypertension. Similarly, leptin action increasing sympathetic activity has been proposed to be involved in mechanisms of hypertension. The aim of this study was to analyze the effects of DA, norepinephrine (NE), and prolactin on leptin release and leptin gene ( OB ) expression in adipocytes from obese and hypertensive patients. Methods Leptin release and OB gene expression were analyzed in cultured adipocytes from 16 obese and hypertensive patients treated with DA (0.001, 0.01, 0.1, and 1.0 μmol/L), NE (1.0 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L), and from five nonobese and normotensive controls treated with DA (1 μmol/L), NE (1 μmol/L), insulin (0.1 μmol/L), and prolactin (1.0 μmol/L). Results A dose-related reduction of leptin release and OB gene messenger ribonucleic acid expression under different doses of DA was observed in adipocytes from obese hypertensive patients. Whereas prolactin treatment elicited a significant increase of both leptin release and OB gene expression, NE reduced these parameters. Although similar effects of DA and NE were observed in adipocytes from controls, baseline values in controls were reduced to 20% of the value in adipocytes from obese hypertensive patients. Conclusion These results suggest that DAergic deficiency contributes to metabolic disorders linked to hyperleptinemia in obese and hypertensive patients.

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Bromocriptine inhibits norepinephrine release

Cited by 84 publications

References 4 publications

Bromocriptine Reduces Obesity, Glucose Intolerance and Extracellular Monoamine Metabolite Levels in the Ventromedial Hypothalamus of Syrian Hamsters

Bromocriptine Reduces Obesity, Glucose Intolerance and Extracellular Monoamine Metabolite Levels in the Ventromedial Hypothalamus of Syrian Hamsters

Intracerebroventricular Administration of Bromocriptine Ameliorates the Insulin-Resistant/Glucose-Intolerant State in Hamsters

Effects of dopamine on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients

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