Vitamins 696x496 1

Vitamin B6 Prolactin

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Bits prolactin release and to compare this effect to that of bromocriptine, a known suppressor of prolactin release, a study was conducted in male rats. Animals were pretreated with pyridoxine hydrochloride, pyridoxal hydrochloride, saline, or bromocriptine 30 min prior to receiving varying doses of chlorpromazine hydrochloride. Blood samples collected 60 min later were also analyzed for serum prolactin.

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Control of the secretion of anterior pituitary hormones has been widely studied in the past few years.1 The hypothalamic dopaminergic pathways have been shown to be involved in the regulation of prolactin, growth hormone, ACTH, and gonadotropins.2 Pyridoxine (vitamin B 6 ) is one of the natural precursors of pyridoxal-5′-phosphate coenzyme in the decarboxylation and transamination of amino acids. As a coenzyme of dopa decarboxylase, this vitamin can induce the transformation of dopa to dopamine, thus sharing the endocrine effects of this amine.


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The acute intravenous administration of B 6 (300 mg pyridoxine chloride and 10 mg pyridoxal 5 — phosphate) on the circulating levels of pituitary hormones was investigated in humans under normal and pathologic conditions.
The effect of Beon PRL and GH release was abolished after 3 day pretreatment with sulpiride; this finding suggests a dopaminergic mediation. In hypothalamo-pituitary diseases the response to Be was found altered: the inhibition of serum PRL was diminished in normo- or hyperprolactinemic women with galactorrhea and disturbed menses but without X-ray evidence of pituitary tumor. When PRL or GH secreting adenomas were present, the responses of PRL and GH to Be were absent or paradoxical.
Our observations support the hypothesis that in normal subjects Be activates hypothalamic aromatic-L-aminoacid-decarboxylase with a consequent increase of dopamine concentration. The lack of response to Be observed in hypothalamo-pituitary disorders might be attributed either to an abnormal response of the pituitary to dopamine or to a reduced ability of the coenzyme to promote the synthesis of this neurotransmitte.

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Journal Of Pharmaceutical Sciences

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