Endocrinology, Vol 115, 1157-1163, Copyright © 1984 by Endocrine Society

ARTICLES

Endocrine role of the decidual tissue: decidual luteotropin regulation of luteal adenylyl cyclase activity, luteinizing hormone receptors, and steroidogenesis

G Gibori, B Kalison, R Basuray, MC Rao and M Hunzicker-Dunn

We have recently reported that the decidual tissue of pseudopregnant and pregnant rats produces a luteotropic substance, decidual luteotropin, which can sustain luteal function in the absence of PRL. However, the luteotropic activity of the decidua depends on the presence of LH in the circulation. The objective of the present investigation was to determine whether decidual luteotropin sustains luteal function by maintaining the luteal cell content of LH receptors and LH-responsive adenylyl cyclase. Pseudopregnant adult rats had their uteri scratched on day 5 to induce decidual tissue formation. Both day 5 hysterectomized and intact pseudopregnant animals were used as controls. On day 7, rats were injected with 0.4 mg 2-bromo-ergocryptine (CB-154) to suppress PRL secretion. Within 48 h, CB-154 administration to either control group not possessing decidual tissue induced a dramatic decrease in progesterone production, LH receptor content, and LH-stimulated adenylyl cyclase in luteal cells. In contrast, suppression of PRL secretion in rats with decidualized uteri had no effect on progesterone secretion, luteal cell LH receptor content, or LH-stimulated adenylyl cyclase. Removal of the decidual tissue immediately after CB-154 treatment caused a significant decline in LH receptors, whereas administration of PRL to control rats without decidual tissue reversed the detrimental effect of CB-154 on both receptor content and LH-stimulated adenylyl cyclase. Examination of the time course (0, 24, and 48 h) of CB-154 action in rats lacking decidual tissue indicated that the decrease in serum progesterone preceded any detectable loss in luteal LH receptor content and LH-stimulated adenylyl cyclase activity. The results also suggest that the decline in LH-stimulated cyclase activity is largely due to the decrease in LH- binding sites and not to an alteration in the cyclase system. PRL withdrawal does not decrease but, rather, enhances epinephrine- stimulated cyclase activity. In summary, results of these investigations have revealed that decidual luteotropin can maintain the luteal content of LH receptors and LH-responsive cyclase and can sustain luteal cell production of progesterone in the absence of PRL; the synergism between decidual luteotropin (or PRL) and LH on luteal steroidogenesis involves more than the maintenance of LH receptors; and PRL withdrawal has opposite effects on LH- and catecholamine-responsive adenylyl cyclases, decreasing the former and stimulating the latter.

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