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T S Sakhatskaia

Publications and source records attributed to T S Sakhatskaia.

2 recordsLinked to original sources

[The effect of ACTH and chorionic gonadotropin on cyclic 3',5'-adenosine monophosphate concentration and of a homogenate of fetal hypophysis on adrenal steroidogenesis in human embryos and fetuses from the 7th to the 12th week of embryonic development].

It was shown that homogenates of the hypophysis of human fetuses from the 8th to the 12th week of gestation stimulated in vitro formation of F and DEA-sulfate in the adrenal glands of fetuses of the same gestation period. ACTH increased the cAMP concentration in the adrenal glands of all the embryos and fetuses under study; this pointed to the presence in them of ACTH-dependent adenylcyclase, and, consequently, of the ACTH receptors. On the contrary, chorionic hormone produced no effect on the cAMP concentration in the adrenal glands. The data obtained, together with those published earlier suggested that adrenal glands of human fetuses from the 8th week of gestation were already under the controlling influence of ACTH of their hypophyses and that the action mechanism of ACTH on the adrenal glands of fetuses was analogous to its action on the adrenal glands of adult.

Adrenal Glands

[Effect of ACTH on the transformation of progesterone by the adrenal glands of human fetuses in vitro].

It was shown in vitro that ACTH influenced the progesterone transformation increasing corticosterone production only in those fetuses whose adrenal glands, in the absence of ACTH, transformed progesterone chiefly into hydrocortisone (8--12-week fetuses). But exogenous ACTH failed to influence such transformation of progesterone in 17--24-week fetuses in which the adrenal glands, in the absence of ACTH preparation, produced an equal amount of hydrocortisone and corticosterone. The results obtained and also the data on ACTH content in the hypophysis and the blood of human fetuses at various periods of prenatal development indicated that the changes in progesterone transformation occurring with the advance of fetal age was caused by endogenous ACTH.

Adrenal Glands