Luteinizing hormone/follicle-stimulating synthesis

The episodic secretion of the hypothalamic hormone, gonadotrophin-releasing hormone (GnRH), stimulates synthesis and release of the gonadotrophins. LH (luteinizing hormone) and FSH (follicle-stimulating hormone), from the anterior pituitary. Despite the names, both gontidotrophins act cooperatively on the ovaries in the woman and the testes in the man to stimulate sex hormone secretion and reproductive processes. 

Thyrotropin (thyroid-stimulating hormone, TSH) and the related hormones lutropin (luteinizing hormone, LH) and follitropin (follicle-stimulating hormone, FSH) originate in the adenohypophysis. They are all dimeric glycoproteins with masses of around 28 kDa. Thyrotropin stimulates the synthesis and secretion of thyroxin by the thyroid gland. 

Mechanism of Action A testosterone derivative that suppresses the pituitary-ovarian axis by inhibiting the output of pituitary gonadotropins. Causes atrophy of both normal and ectopic endometrial tissue in endometriosis. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are depressed in fibrocystic breast disease. Inhibits steroid synthesis and binding of steroids to their receptors in breast tissues. Increases serum levels of esterase inhibitor. Therapeutic Effect Produces anovulation and amenorrhea, reduces the production of est rogen, corrects biochemical deficiency as seen in hereditary angioedema. 

Digitalis has effects on sex hormones. It causes increased serum concentrations of follicle-stimulating hormone (FSH) and estrogen and reduced concentrations of luteinizing hormone (LH) and testosterone (89-92). These effects are probably not related to any direct estrogen-like structure of digitalis (despite structural similarities), but rather to an effect involving the synthesis or release of sex hormones. There are three possible clinical outcomes of these effects. 

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