Effect Of Bromocriptine Treatment Research Articles

The effect of bromocriptine treatment on sexual functioning and depressive symptoms in women with mild hyperprolactinemia.

Elevated prolactin levels are associated with sexual dysfunction in women. No previous study has investigated the effect of dopamine agonists on sexual functioning in women. The study enrolled 30 young women with mild hyperprolactinemia (serum prolactin levels in the range between 25 and 50ng/mL), 15 of whom were later treated with bromocriptine (5-10mg daily), as well as 14 age- and weight-matched healthy women. All women completed a questionnaire evaluating female sexual function (Female Sexual Function Index - FSFI) and a questionnaire evaluating the presence and severity of depressive symptoms (Beck Depression Inventory Second Edition - BDI-II). Women with mild hyperprolactinemia had a lower total FSFI score, lower scores in all domains of sexual functioning (desire, arousal, lubrication, and dyspareunia), as well as a lower total BDI-II score than control women. Bromocriptine increased the FSFI score and tended to reduce BDI-II score. Moreover, the drug normalized desire, arousal, lubrication and dyspareunia, as well as improved orgasm and sexual satisfaction and this action correlated with changes in prolactin levels and an improvement in insulin sensitivity. No changes in sexual functioning and depressive symptoms were observed in untreated women with mild hyperprolactinemia and healthy controls. Bromocriptine treatment improves female sexual functioning and slightly affects depressive symptoms in women with elevated prolactin levels and this effect is related to its prolactin-lowering and metabolic effects.

The effects of bromocriptine treatment during early pregnancy on postpartum maternal behaviors in rats.

Prolactin, a hormone of the anterior pituitary, is involved in initiating maternal behavior, alleviating postpartum anxiety, and stimulating lactogenesis. Bromocriptine, a dopamine D2 receptor agonist, inhibits prolactin secretion. Bromocriptine administration represses postpartum maternal behaviors (pup retrieval) in mice, and causes elevated anxiety in the elevated plus maze [Larsen & Grattan (2010). Endocrinology 151(8): 3805-3814]. Whether similar effects exist in other species is unknown. The present study examined the possible involvement of prolactin during early gestation on maternal behavior and anxiety in rats. Bromocriptine given on days 2-4 of pregnancy resulted in impaired postpartum maternal behaviors in a novel environment during early lactation. However, compared to controls, bromocriptine-treated subjects did not exhibit increased postpartum anxiety in the elevated plus maze. These findings support work in mice that bromocriptine treatment during early gestation impedes postpartum maternal care, and indicate that early gestational hormonal status affects postpartum behavior more broadly in other mammals.

Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

Weighted Effects of Bromocriptine Treatment on Glucose Homeostasis during Hyperglycemic versus Euglycemic Clamp Conditions in Insulin Resistant Hamsters: Bromocriptine as a Unique Postprandial Insulin Sensitizer

P.3.c.045 The effect of bromocriptine treatment on antipsychotic drug-induced hyperprolactinemia

P.3.c.045 The effect of bromocriptine treatment on antipsychotic drug-induced hyperprolactinemia

Bromocriptine for infertile males with mild hyperprolactinemia: hormonal and spermatogenic effects.

To clarify the influence of hyperprolactinemia on spermatogenesis and steroidogenesis in infertile male patients, the serum prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol concentrations were and the effect of bromocriptine treatment on spermatogenesis was examined. A total of 1234 patients were evaluated and 147 men had hyperprolactinemia. Of these, only 30 had PRL concentrations more than twice the upper limit of normal and most of them had a little excess over the upper limit. For 10 of these 30, serum hormone concentrations were measured and semen was analyzed before and after bromocriptine administration. No relationship between the PRL and other hormone concentrations was found. No changes were noted in the LH, FSH, testosterone, or estradiol concentrations, or in the sperm density and motility after treatment. The mean PRL decreased from 26.5 +/- 4.5 to 1.4 +/- 1.8 ng/mL. In infertile men who are mildly hyperprolactinemic, bromocriptine administration does not improve semen analysis, although it does normalize the PRL.

Effects of bromocriptine treatment on the expression of sexual behavior in male sheep (Ovis aries)2

Twenty-three rams were treated twice daily with subcutaneous injections of bromocriptine or vehicle over 30 d during two seasons, spring and fall. Sexual behavior was observed and quantified to determine the effects of bromocriptine-induced hypoprolactinemia on mount attempt (MA), mount (M), and ejaculation (E) frequency of the rams upon exposure to estrous ewes. Behavioral responses and serum prolactin (PRL) concentrations were determined on a weekly basis before, during, and after the treatment period in each season. Treatment with bromocriptine caused a significant decrease in serum concentrations of PRL during both seasons (P < .01). Post-treatment period concentrations of PRL returned to pretreatment levels during the spring, whereas during the fall, post-treatment period PRL concentrations remained low (P < .05). The frequency of MA and M was lower during bromocriptine treatment relative to control rams in the spring (P < .05). The frequency of MA and M returned to pretreatment values after bromocriptine treatment was withdrawn. Ejaculation frequency tended to decrease during and after bromocriptine treatment relative to controls (P < .09). There was no effect of bromocriptine treatment on frequency of MA and M during the fall. During the fall, the frequency of E tended to decrease in bromocriptine-treated rams (P < .1). These data indicate that bromocriptine-induced hypoprolactinemia is associated with a significant diminution in expression of sexual behavior in rams. It is suggested that PRL modulates the intensity of expression of sexual behavior in rams, and this effect may be season-dependent.

Therapeutic effect of the D 2-dopamine agonist bromocriptine on acute and relapsing experimental allergic encephalomyelitis

We examined the effect of bromocriptine (BCR) treatment on the duration and severity of neurological symptoms of acute experimental allergic encephalomyelitis (EAE), an animal model for demyelinating diseases, particularly multiple sclerosis. To mimic the clinical situation, BCR treatment was started after the onset of clinical signs. Furthermore, the effect of BCR treatment on the course of a chronic relapsing form of EAE was studied. BCR was injected at daily intervals in a dose that resulted in sustained suppression of plasma concentrations of prolactin, a pituitary hormone that plays a role in immunoregulation. In acute EAE, BCR therapy reduced both severity and duration of the clinical signs. In chronic relapsing EAE, BCR treatment did not affect the severity and duration of the first attack, but reduced the duration of the subsequent, second attack. Thus, BCR treatment improves the clinical course in animals with ongoing disease. These findings may have implications for the search for new therapeutic approaches in multiple sclerosis.

Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics

Obese postmenopausal female volunteers were given timed daily oral dosages of bromocriptine, and tested for reduction of body fat stores. This dopamine agonist has been shown to reset circadian rhythms that are altered in obese animals and to reduce body fat levels in several animal models. The participants were instructed not to alter their existing exercise and eating behavior during treatment. Skinfold measurements were taken on 33 subjects as indices of body fat. The measurements (e.g., suprailiac) were reduced after six weeks by about 25%, which represents a reduction of 11.7% of the total body fat. These dramatic decreases in body fat, which are equivalent to that produced by severe caloric restriction, were accompanied by more modest reductions of body weight (2.5%), indicating a possible conservation of protein that is usually lost as a consequence of such caloric restriction. The effects of bromocriptine treatment on body fat and hyperglycemia were also examined in non-insulin dependent diabetics being treated with oral hypoglycemics (7 subjects) or insulin (7 subjects). Total body fat was reduced by 10.7% and 5.1% in diabetics on oral hypoglycemics and insulin, respectively, without any significant reductions in body weight. Hyperglycemia was reduced in most of the 15 diabetic subjects treated leading to euglycemia and even cessation of hypoglycemic drugs in 3 of the 7 subjects during 4-8 weeks of bromocriptine treatment. These findings support the hypothesis that obesity and type II diabetes may be treated effectively with bromocriptine when administered at the proper times and dosages.

A Characterization of Estrogen’s Influence on Anterior Pituitary Androgen Receptor: Effect of Bromocriptine Treatment

The action of gonadal steroids are mediated through the binding to specific intracellular receptors. Our recent studies have demonstrated that estrogen (E) treatment will increase the concentration of cytosolic androgen receptor (AR) in the anterior pituitary (AP) gland perhaps reflecting in increased sensitivity of this tissue circulating androgen. However, chronic E treatment also increases AP weight and cell number. Consequently, the following studies were performed to determine the relationship between increases in AP cytosolic AR and increases in AP weight following chronic E treatment. Gonadectomized male and female Fischer 344 (F344) rats were implanted with a 5-mm Silastic capsule of 17 beta-estradiol. Control animals were sham implanted. Animals were sacrificed at 1, 3, 7 and 21 days after the commencement of E treatment and AP glands were weighed and processed for cytosolic AR and nuclear estrogen receptor (ER) content. AR and ER were determined by in vitro binding assays using 3H-dihydrotestosterone and 3H-estradiol, respectively. AP weight increased significantly by 3 days of E treatment in females and by 7 days in males (p less than 0.05). However, AP weight of E-treated males was significantly less than females throughout (p less than 0.05). Significant increases in AP cytosolic AR content (fmol bound/gland) were detected within 1 day of E treatment to female rats but not until 7 days in male rats. AP cytosolic AR content peaked at 7 days of E treatment in females and 21 days in males. AP cytosolic AR concentration (expressed as per milligram cytosol protein) peaked 3 days after E at which time there were significant E effects in both males and females.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Bromocriptine Treatment on Immune Responses and 3–Methylcholanthrene-Induced Tumorigenesis in Rats

Seven-week-old male Sprague-Dawley rats were given a single injection of 1.5 mg of 3-methylcholanthrene (3MC) to induce in situ fibrosarcomas. The rats were also treated with the dopamine agonist bromocriptine (BCR) from two days prior to 14 days after 3MC treatment and again for 14 consecutive days beginning at week 5. Tumor incidence was markedly increased and latency decreased in BCR-3MC rats compared to 3MC controls. Natural killer (NK) cell cytotoxicity responses and production of interleukin 2 (IL2) was enhanced at two weeks in rats treated with only BCR. Natural killer cell activity was suppressed at two weeks in rats treated with only 3MC. This effect was reversed by BCR treatment. Rats treated with 3MC and BCR had suppressed NK cell responses and production of IL2 and interferon-gamma (IFN) at 12 weeks. In another study, rats injected with 1, 3 or 5 mg/kg BCR for 14 consecutive days had increased NK cell activity and IL2 production at all doses and increased IFN production at the two high doses. Antibody (IgG) responses to an injected antigen and delayed-type hypersensitivity reactions were not affected by BCR treatment. Animals treated with the two high doses of BCR had decreased serum prolactin (PRL) levels. Serum growth hormone (GH) concentrations were markedly increased in the group treated with 3 mg/kg BCR. These data suggest that BCR enhances 3MC-induced tumorigenesis. The mechanism of this effect is apparently not mediated by suppression of the immune system since BCR-treated rats had selectively enhanced immune function. Enhancement of immune responses by BCR has not been previously reported.

Lymphocyte Abnormalities in Patients with Macro- and Micro-Prolactinoma: Different Effects of Bromocriptine Treatment in the two Groups

Lymphocyte Abnormalities in Patients with Macro- and Micro-Prolactinoma: Different Effects of Bromocriptine Treatment in the two Groups

Transient hyperprolactinemia during cycle stimulation: Influence on the endocrine response and fertilization rate of human oocytes and effects of bromocriptine treatment

International Journal of Gynecology & ObstetricsVolume 27, Issue 3 p. 476-476 Citations from the literature fertility and sterility Transient hyperprolactinemia during cycle stimulation: Influence on the endocrine response and fertilization rate of human oocytes and effects of bromocriptine treatment A Reinthaller, A ReinthallerSearch for more papers by this authorC Bieglmayer, C BieglmayerSearch for more papers by this authorJ Deutinger, J DeutingerSearch for more papers by this authorP Csaicsich, P CsaicsichSearch for more papers by this author A Reinthaller, A ReinthallerSearch for more papers by this authorC Bieglmayer, C BieglmayerSearch for more papers by this authorJ Deutinger, J DeutingerSearch for more papers by this authorP Csaicsich, P CsaicsichSearch for more papers by this author First published: December 1988 https://doi.org/10.1016/0020-7292(88)90138-5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume27, Issue3December 1988Pages 476-476 RelatedInformation

Effects of bromocriptine on prolactin cellular hypertrophy, proliferation and secretory activity in diethylstilbestrol-induced pituitary tumors

Pituitary tumors induced by chronic diethylstilbestrol (DES) treatment in female F344 rats were treated subsequently with bromocriptine (BC). Effects of BC on separable subpopulations of lactotrophs were examined. Enzymatically dissociated cells from individual pituitaries were assessed regarding total number, relative lactotroph population, intracellular prolactin (PRL) content, PRL release in primary culture, and density alterations by separation in Ficoll-Hypaque or after sedimentation at unit gravity. In addition to the treatment and analysis of in situ tumors, the effects of BC treatment in vitro were assessed, using tumor cells which were first separated on Ficoll-Hypaque. Cell proliferation was assessed by cell cycle analysis, using DNA measurement by laser flow cytometry. BC treatment of tumors reversed the effects of DES on pituitary weight, PRL content and in vitro PRL release. Total cell recovery was not affected by BC, but cell separation showed that BC reduced the number of larger PRL-containing cells. Cell cycle analysis showed a decrease in numbers of cells in S and G 2 cycle phases after BC in only one of four experiments. BC had an effect on proliferation in only the upper gradient fractions, containing the smallest cells. Culture of Ficoll-separated tumor cells revealed greater PRL release among lighter/smaller cells. BC treatment inhibited PRL release from both light and dense cells. The results establish that PRL cell hypertrophy, as well as hyperplasia, results from DES treatment. Bromocriptine treatment reverses this hypertrophy concomitant with inhibiting PRL synthesis and release. Reversal of proliferation in tumor cells is not a major effect of bromocriptine treatment.

Transient hyperprolactinemia during cycle stimulation: influence on the endocrine response and fertilization rate of human oocytes and effects of bromocriptine treatment

The effect of transient hyperprolactinemia and its treatment during cycle stimulation on the endocrine response and fertilization rate of human oocytes was studied. Fifty stimulated cycles were included in the study and divided into three groups: group I consisted of 18 cycles with serum prolactin (PRL) levels less than or equal to 25 ng/ml; group II contained 15 cycles, where patients developed PRL levels greater than 25 ng/ml; group III consisted of 17 cycles, where patients, who already developed hyperprolactinemia in a previous cycle, were treated by 3.75 mg bromocriptine daily. The serum estradiol (E2), progesterone (P) and PRL levels 1, 2, and 3 days before and at oocyte retrieval were evaluated. The E2 decrease at oocyte retrieval was significantly steeper in groups I and III. Follicular luteinization was more effective in groups I and III. The fertilization rate in groups I and III was significantly higher than in group II. High serum PRL levels seem to interfere in follicular and oocyte development. The treatment of transient hyperprolactinemia improved the patients' endocrine response and the fertilization rate of oocytes.

Effect of Bromocriptine Treatment on the Fibrous Tissue Content of Prolactin-Secreting and Nonfunctioning Macroadenomas of the Pituitary Gland

We performed a quantitative study using a point-counting technique at the light microscope level of the fibrous tissue content of PRL-secreting and nonfunctioning pituitary macroadenomas from patients treated or untreated with bromocriptine (BC) before surgery. There was a significant increase in the fibrous tissue content of PRL-secreting, but not nonfunctioning, tumors after BC treatment. The extent of the increase in fibrous tissue in prolactinomas correlated with the duration of treatment with BO.

T-cell dysregulation in patients with hyperprolactinemia: Effect of bromocriptine treatment

We studied four patients with tumoral hyperprolactinemia and normal ovarian function before and after prolactine levels had become normal with treatment with bromocriptine (BrC), a dopamine agonist that inhibits prolactin release. Their proliferative responses to concanavalin A, pokeweed mitogen, and, to a lesser extent, phytohemagglutinin, their spontaneous and concanavalin A-induced suppression, and their production of interleukin 2 were found to be decreased and to correct partially or completely after bromocriptine treatment. The T-cell response to interleukin 2 was low in two patients in whom it increased after BrC treatment. These findings give insight on the immunomodulatory role of prolactin in vivo.

Effect of bromocriptine treatment on the aldosterone response to angiotensin II and adrenocorticotropin in idiopathic hyperaldosteronism.

Bromocriptine can prevent an increase in plasma aldosterone during the infusion of angiotensin II in normal subjects and during upright posture in some patients with idiopathic hyperaldosteronism. To determine if bromocriptine prevents the increase in plasma aldosterone concentration during angiotensin II infusion in idiopathic hyperaldosteronism, we infused angiotensin II in five patients with idiopathic hyperaldosteronism, before and after treatment with bromocriptine (2.5 mg, three times daily for 5 days), and measured the resulting plasma aldosterone and angiotensin II concentrations. We also determined the adrenal response to ACTH infusion before and after bromocriptine treatment in four of these patients. Bromocriptine treatment did not significantly change the plasma concentrations of aldosterone before or during the infusions of angiotensin II and ACTH. It did significantly decrease mean blood pressure and increase the plasma corticosteroid concentrations in the preinfusion periods, but it did not alter the response of blood pressure to angiotensin II or of plasma corticosteroid concentrations to the ACTH infusions.

Prolactinomas in men: clinical characteristics and the effect of bromocriptine treatment.

Thirty-seven men with prolactin (PRL) producing pituitary adenomas were studied to elucidate if patient's delay might cause the predominance of large tumours in men as compared to women in whom microadenomas predominate. We found two clinical subgroups; one presented with short duration of symptoms, dominated by local signs from the growth of notably large tumours, the other exhibited a long history of disease with hypogonadism as the dominating symptom. There was a correlation between tumour size and PRL levels. The age at the time of diagnosis showed no correlation to duration of symptoms, size of adenoma or PRL levels. Four patients with small adenomas, moderate hyperprolactinemia and short duration of symptoms showed signs of hypergonadotropic hypogonadism. Surgery or irradiation, performed in 14 patients, did not normalize PRL levels. Bromocriptine was equally beneficial in the two clinical subgroups, improving clinical symptoms and normalizing PRL levels in all but three patients. The study shows that the predominance of large tumours in men does not depend on patient's or doctor's delay, but on a high frequency of presumably rapidly growing PRL producing tumours. In the majority of patients, these tumours do not give signs of hypogonadism before the tumour is revealed by local signs of tumour growth.

Accumulation of amyloid in pituitary adenomas.

The accumulation of amyloid in pituitary adenomas was examined in relation to the types of adenoma and the effect of bromocriptine treatment. Amyloid had accumulated in 34 of 48 adenomas (71%). The occurrence in prolactin-secreting adenomas and growth hormone-secreting adenomas was 79%, respectively, while that in non-functioning adenomas was 50%. Treatment with bromocriptine enhanced the occurrence and extent of the amyloid accumulation in prolactin- or growth hormone-secreting adenomas. Electron microscopy revealed the initial appearance of the amyloid fibrils in the smooth endoplasmic reticulum and a possible sequential process of their release from the cells. The presence of secretory granules in vesicles containing amyloid fibrils and their simultaneous release with amyloid fibrils suggested that degradation of secretory granules was involved in the formation of amyloid.

Effect of bromocriptine treatment on male infertility associated with hyperprolactinemia.

Hyperprolactinemia associated with male infertility or impotence was found in ten patients. Mean prolactin level was 83 +/- 49 ng/ml (range 46-26- ng/ml). The etiological bases of the hyperprolactinemia were a microadenoma in one patient, liver disease in two, and idiopathic in seven patients. Bromocriptine treatment, 2.5-7.5 mg daily for 8-16 weeks lowered prolactin to normal levels in all patients. Three oligoasthenospermic subjects showed a marked increase in sperm motility; their wives conceived within 5-8 weeks of treatment after longstanding infertility. Two of these women gave birth to normal babies and one aborted in the first trimester of pregnancy. The mechanism by which hyperprolactinemia interferes with sperm production and the effect of bromocriptine on this mechanism is discussed.