Dopamine-prolactin

[zkt]

I`ve read somewhere, maybe more than on place, that PRL is antagonist of DA. My experiments with cabergoline seem to bear this assumption out at least as regards attention, excitement and libido.
A handfull of studies would be helpful but Ill take what I can get.

 

[Kwirion]

Excellent article about Cabergoline Cabergoline (Dostinex) Profile

More about: http://www.antiaging-systems.com/a2z/cabergoline_dostinex.htm

Cabergoline treatment in men with psychogenic erectile dysfunction: a randomized, double-blind, placebo-controlled study.
Nickel M, Moleda D, Loew T, Rother W, Pedrosa Gil F.
Clinic for Psychosomatic, Inntalklinik, Simbach/Inn, Germany. m.nickel@inntalklinik.de
Abstract
The effectiveness of cabergoline in 50 men with psychogenic erectile dysfunction was investigated in a 4-month, randomized, placebo-controlled, double-blind study with validated psychological tests, and prolactin, follicle-stimulating hormone, luteinizing hormone and testosterone serum levels. Cabergoline treatment was well-tolerated and resulted in normalization of hormone levels in most cases. In the cabergoline-treated group, significant interactions between prolactin and testosterone serum concentrations were observed. Erectile function improved significantly. Sexual desire, orgasmic function, and the patient's and his partner's sexual satisfaction were also enhanced. Cabergoline may be an effective and safe alternative agent for men with psychogenic ED.
PMID: 16728967 [PubMed - indexed for MEDLINE]

Endocr Pract. 2010 May 3:1-13. [Epub ahead of print]
Achievement of fertility in an infertile man with resistant macroprolactinoma using high dose of bromocriptine and a combination of hCG and an aromatase inhibitor.
Heidari Z, Hosseinpanah F, Shirazian N.
Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Science, Tehran, Iran.
Abstract
Objective: To describe achievement of fertility in an infertile man with resistant macroprolactinoma using high dose of bromocriptine and a combination of hCG and an aromatase inhibitor. METHODS: We present historical features and results of clinical, laboratory and imaging evaluation in a man with infertility due to resistant macroprolactinoma. RESULTS: we report a case of macroprolactinoma in a 36 year-old infertile man who failed to attain normal serum testosterone level and fertility on either bromocriptine or cabergoline. Testosterone replacement or human chorionic gonadotropine (hCG) therapy in this patient resulted in a rise of prolactin (PRL) levels, which declined following therapy discontinuation. The combination of high doses of bromocriptine, hCG and an aromatase inhibitor facilitated near normalization of PRL levels, shrinkage of adenoma, recovery of serum testosterone level, sexual function, sperm count and achievement of fertility. CONCLUSION: aromatase inhibitor may facilitate successful testosterone replacement therapy in male patients with prolactinoma.
PMID: 20439242 [PubMed - as supplied by publisher]

Eur J Endocrinol. 2009 Jul;161(1):163-9. Epub 2009 Apr 9.
Recovery of persistent hypogonadism by clomiphene in males with prolactinomas under dopamine agonist treatment.
Ribeiro RS, Abucham J.
Division of Endocrinology, Department of Medicine, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Pedro de Toledo, 910. São Paulo 04039-002, Brasil.
Abstract
CONTEXT: Persistence of hypogonadism is common in male patients with prolactinomas under dopamine agonist (DA) treatment. Conventional therapy with testosterone causes undesirable fluctuations in serum testosterone levels and inhibition of spermatogenesis. OBJECTIVE: To evaluate the use of clomiphene as a treatment for persistent hypogonadism in males with prolactinomas. DESIGN: Open label, single-arm, prospective trial. PATIENTS: Fourteen adult hypogonadal males (testosterone <300 ng/dl and low/normal LH) with prolactinomas on DA, including seven with high prolactin (range: 29-1255 microg/l; median: 101 microg/l) despite maximal doses of DA. INTERVENTION: Clomiphene (50 mg/day orally) for 12 weeks. MEASURES: Testosterone, estradiol, LH, FSH, and prolactin were measured before and 10 days, 4, 8, and 12 weeks after clomiphene. Erectile function, sperm analysis, body composition, and metabolic profiles were evaluated before and after clomiphene. RESULTS: Ten patients (71%), five hyperprolactinemic and two normoprolactinemic, responded to clomiphene (testosterone >300 ng/dl). Testosterone levels increased from 201+/-22 to 457+/-37 ng/dl, 436+/-52, and 440+/-47 ng/dl at 4, 8, and 12 weeks respectively (0.001<P<0.01). Estradiol increased significantly and peaked at 12 weeks. LH increased from 1.7+/-0.4 to 6.2+/-2.0 IU/l, 4.5+/-0.7, and 4.6+/-0.7 IU/l at 4, 8, and 12 weeks respectively (0.001<P<0.05). FSH levels increased in a similar fashion. Prolactin levels remained unchanged. Erectile function improved (P<0.05) and sperm motility increased (P<0.05) in all six patients with asthenospermia before clomiphene. CONCLUSIONS: Clomiphene restores normal testosterone levels and improves sperm motility in most male patients with prolactinomas and persistent hypogonadism under DA therapy. Recovery of gonadal function by clomiphene is independent of prolactin levels.
PMID: 19359408 [PubMed - indexed for MEDLINE]

Cabergoline treatment rapidly improves gonadal function in hyperprolactinemic males: a comparison with bromocriptine
by
De Rosa M, Colao A, Di Sarno A, Ferone D,
Landi ML, Zarrilli S, Paesano L, Merola B, Lombardi G.
Department of Endocrinology and Molecular and Clinical Oncology,
Federico II University, Naples, Italy.
Eur J Endocrinol 1998 Mar;138(3):286-93

ABSTRACT
This study evaluated the effects of chronic treatment with cabergoline (CAB), a new, potent and long-lasting ergoline-derived dopamine agonist, on seminal fluid parameters and sexual and gonadal function in hyperprolactinemic males in comparison with the effect of bromocriptine (BRC) treatment. Seventeen males with macroprolactinoma were treated with CAB at a dose of 0.5-1.5 mg/week (n = 7), or BRC at a dose of 5-15 mg/day (n = 10) for 6 months. Baseline prolactin (PRL) was 925.7 +/- 522.6 microg/l in the CAB-treated group and 1059.4 +/- 297.6 microg/l in the BRC-treated group. All the patients suffered from libido impairment, ten from reduced sexual potency, and six had infertility. In five patients provocative bilateral galactorrhea was found. Seminal fluid analysis, functional seminal tests and penis rigidity and tumescence, measured by nocturnal penile tumescence (NPT) using Rigiscan equipment, were assessed before and after 1, 3 and 6 months of CAB or BRC treatment. Hormone profiles were assessed before and after 15, 30, 60, 90 and 180 days of both treatments. Before treatment, all patients had a low sperm count with oligoasthenospermia, reduced motility and rapid progression with an abnormal morphology and decreased viability, and a low number of erections. After 1 month, serum PRL levels were significantly reduced in both groups of patients (20.6 +/- 6.6 microg/l during CAB and 256.3 +/- 115.1 microg/l during BRC treatment) and were normalized after 6 months in all patients (CAB: 7.9 +/- 2.2 microg/l; BRC: 16.7 +/- 1.8 microg/l). After 6 months, a significant increase of number, total motility, rapid progression and normal morphology was recorded in patients treated with both CAB and BRC. An increase in the number of erections during the first 3 months of both treatments was noted by NPT. However, the improvements in seminal fluid parameters and sexual function were more evident and rapid in patients treated with CAB. The number of erections was normalized after 6 months of treatment in all patients submitted to CAB treatment, and in all patients but one treated by BRC. In addition, a significant increase of serum testosterone (from 3.7 +/- 0.3 to 5.3 +/- 0.2 microg/l) and dihydrotestosterone (from 0.4 +/- 0.1 to 1.1 +/- 0.1 nmol/l) was recorded. At the beginning of treatment, mild side-effects were recorded in two patients after CAB and mild-to-moderate side-effects in five patients after BRC administration. The treatment with CAB normalized PRL levels, improving gonadal and sexual function and fertility in males with prolactinoma, earlier than did BRC treatment, providing good tolerability and excellent patient compliance to medical treatment.

Mucuna pruriens lowers PRL too: Mucuna pruriens: more testosterone, more LH, less prolactin

 

[OhNoYo]

I`ve read somewhere, maybe more than on place, that PRL is antagonist of DA. My experiments with cabergoline seem to bear this assumption out at least as regards attention, excitement and libido.
A handfull of studies would be helpful but Ill take what I can get.

Prolactin (PRL) is not necessarily speaking in medical terms an antagonist of dopamine (DA), b/c that would consist of PRL working as an antagonist on DA receptors, which is NOT the case.

However, one may assume that DA & PRL levels r inversely correlated b/c when DA is high, PRL is low. DA is aka Prolactin-Inhibiting-Factor (PIF). So, it can be speculated that high levels of both in the body, at least for extended periods of time, would be highly unlikely. However, having low levels of both in the body seems more possible.

Dopamine: A Prolactin-Inhibiting Hormone -- BEN-JONATHAN 6 (4): 564 -- Endocrine Reviews

Studies on the Mechanism of the Dopamine-Mediated Inhibition of Prolactin Secretion -- MACLEOD and LEHMEYER 94 (4): 1077 -- Endocrinology

 

[OhNoYo]

I`ve read somewhere, maybe more than on place, that PRL is antagonist of DA. My experiments with cabergoline seem to bear this assumption out at least as regards attention, excitement and libido.
A handfull of studies would be helpful but Ill take what I can get.

zkt, provided below is information you mite find informative & interesting in regards to the refractory period, which is an excellent subject to research relating to dopamine-prolactin interaction physiology...

Absence of orgasm-induced prolactin secretion in a healthy multi-orgasmic male subject


http://en.wikipedia.org/wiki/Refractory_period_(sex)

 

[Michael Scally MD]

Check out: Gill-Sharma MK. Prolactin and male fertility: the long and short feedback regulation. Int J Endocrinol 2009;2009:687259. Prolactin and Male Fertility: The Long and Short Feedback Regulation

And: https://thinksteroids.com/community/posts/664438


Ben-Jonathan N, Hnasko R. Dopamine as a Prolactin (PRL) Inhibitor. Endocr Rev 2001;22(6):724-63. http://edrv.endojournals.org/cgi/content/full/22/6/724

Dopamine is a small and relatively simple molecule that fulfills diverse functions. Within the brain, it acts as a classical neurotransmitter whose attenuation or overactivity can result in disorders such as Parkinson's disease and schizophrenia. Major advances in the cloning and characterization of biosynthetic enzymes, transporters, and receptors have increased our knowledge regarding the metabolism, release, reuptake, and mechanism of action of dopamine. Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium fluxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. Thus, PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor. The generation of transgenic animals with overexpressed or mutated genes expanded our understanding of dopamine-PRL interactions and the physiological consequences of their perturbations. PRL release in humans, which differs in many respects from that in laboratory animals, is affected by several drugs used in clinical practice. Hyperprolactinemia is a major neuroendocrine-related cause of reproductive disturbances in both men and women. The treatment of hyperprolactinemia has greatly benefited from the generation of progressively more effective and selective dopaminergic drugs.

 

[Kwirion]

Vitamin D3 can lower prolactin too.
ScienceDirect - Molecular and Cellular Endocrinology : Effects of vitamin D3 metabolites on production of prolactin and growth hormone in rat pituitary cells

Effects of vitamin D3 metabolites on production of prolactin and growth hormone in rat pituitary cells

Institute of Physiology, University of Oslo,
Oslo 1, Norway
2Hormone and Isotope Laboratory, Aker
Hospital, Oslo 5, Norway
3Institute for Nutrition Research, School of
Medicine, University of Oslo, Oslo 3, Norway
Received 10 March 1982; revised 10 May 1982; accepted 10 May 1982.
Available online 24 January 2003.
Abstract

Recent animal studies and tissue-culture studies have led to the suggestion that prolactin (PRL) and growth hormone (GH) are involved in the regulation of 25-hydroxyvitamin d-1?-hydroxylase activity. This study was undertaken to investigate the effects of vitamin D on the production of PRL and GH. A clonal strain of rat-pituitary tumor cells (GH3) that spontaneously synthesize and secrete PRL and GH was used as model system. The hormones were measured by radioimmunoassay, and the amount of hormones that accumulated in the medium during 24 h was used as a measure of prolactin.

Treatment of the GH3 cells with 1?, 25-dihydroxyvitamin D3 (1?, 25-(OH)2D) caused a parallel and dose-dependent decrease in the production of both PRL and GH, and the effects were significant at 10?11 and 10?10 M, respectively. The maximal inhibition (20–40% of controls) by 1?, 25-(OH)2D was obtained at 10?6 M after 6 days of treatment, and the effect was detectable after 2 days. Similar effects were observed with 25-hydroxy-vitamin D3 (25-OHD) and the synthetic analog 1?-hydroxyvitamin D3 (1?-OHD), but the ED50 for these substances were more than 103 times higher than the corresponding concentration of 1?, 25-(OH)2D. In contrast, there was no effect of 24,25-dihydroxyvitamin D3 (24,25-(OH)2D) (10?11?10?6M) on the production of PRL and GH. None of the vitamin D analogs affected cell growth measured as total cell protein. Equimolar concentrations (10?7M) of 25-OHD, 1?-OHD and 24,25-(OH)2D slightly reduced the inhibitory effect of 1?,25-(OH)2D when used in combination.

The stimulatory effects of thyroliberin (TRH) and estrogens on PRL production were partly inhibited by treatment with 1?,25-(OH)2D. GH3 cells pre-treated with 1?,25-(OH)2D had similar TRH and 17?-estradiol-binding characteristics as untreated control cells.

We conclude that, in GH3 cells, 1?,25-(OH)2D reduces the production of PRL and GH and strongly counteracts the actions of TRH and estrogens without affecting receptor affinity and concentration. Our results suggest a feed-back loop between the renal tubular cells and the anterior pituitary.

 

[BBC3]

Does anyone here have any documentation as to what the use of Nandrolone typically does to Prolactin levels....

 

[Kwirion]

Does anyone here have any documentation as to what the use of Nandrolone typically does to Prolactin levels....

From: Cabergoline (Dostinex) Profile

Dostinex will even get rid sexual dysfunction caused by excess prolactin (5) (which is (anecdotally at least) highly correlative with the use of certain steroids like the Nandrolones and Trenbolones (Deca and Tren). This is great news for everyone who loves Tren and Deca, because those two steroids are really great additions to almost any cycle- but many people avoid using them because of the possibility of them causing impotence (often called “deca dick”).

http://www.steroidology.com/forum/anabolic-steroid-forum/77929-does-trenbolone-nandrolone-stimulate-prolactin-production.html
http://www.google.pl/#hl=pl&source=...=f&aqi=&aql=&oq=&gs_rfai=&fp=239d7137087c8d10

 

[Kwirion]

Excellent info / thread about prolactin:
https://thinksteroids.com/community/posts/664507

(Thanks to Scally MD!))