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Regulation of LH receptors

Cyclic AMP is one of the mediators of FSH action on LH receptor induction because dibutyryl cyclic AMP will increase granulosa receptors in vitro. Other factors may also be involved (e.g., oestrogens) because the cyclic AMP analogues were less potent than FSH. Once induced, the continual presence of FSH is required to maintain normal levels of LH receptors [5], [Pg.160]

The role of oestrogens in controlling LH receptor synthesis in the testis is not known but oestradiol receptors are present in rat Leydig cells [39]. Glucocorticoids inhibit the induction of LH receptors corticosteroid receptors have been demonstrated in rat testis [40] and treatment of prepubertal rats [41] and immature hy-pophysectomized rats with corticosteroids decreased the numbers of LH receptors and steroid production. [Pg.160]

After hypophysectomy there is a rapid loss of LH receptors and androgen secretion by the testis. Treatment with LH alone will restore Leydig cell steroidogenesis but also causes even further decreases in testicular LH receptors. Continued treatment with LH alone leads to Leydig cell hyperplasia and an increase in LH receptors. However, even with marked Leydig cell hyperplasia in response to sustained elevations of endogenous LH, as in the tfm rat (see Ref. 6 for other references), the LH receptor content of the testis remains subnormal. [Pg.161]

Prolactin has been shown to increase LH receptor numbers in dwarf mice, seasonally repressed hamsters and hypophysectomized rats (see Ref. 6 for other references). In the hypophysectomized rats the combined effects of prolactin, growth hormone and LH were necessary to maintain the LH receptors [46]. The induction of hyperprolactinemia leads to increased LH receptors. Decreases in serum prolactin levels caused by treatment with compounds that inhibit the release of prolactin (dopamine analogues) decrease LH receptors (see Ref. 6 for other references). [Pg.161]

FSH also increases LH receptor numbers in rat testes but this has only been observed in immature hypophysectomized rats. This effect of FSH can be blocked by administration of oestrogens which is the opposite of their effects in the ovary. The mechanism of action of this effect of FSH on LH receptors is not known. Presumably FSH is acting via stimulation of the Sertoli cells because there are no receptors for FSH on Leydig cells. Paracrine factors secreted by the seminiferous tubules and having a positive effect on Leydig cell function have been demonstrated [4]. The described effects of FSH may have been due to the small amounts of LH contaminating the FSH preparations [47], Treatment with the estimated quantities of LH alone had no effect on the in vitro LH responses [48]. The availability of very pure FSH should now enable workers to determine the exact effect of FSH alone. [Pg.161]


The down regulation of LH receptors which occurs after administration of hCG in vivo to mature rats does not occur in 5-day-old rats. In the latter the LH receptors can be up-regulated [105]. [Pg.175]


See other pages where Regulation of LH receptors is mentioned: [Pg.160]   


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