Influence of morphine treatment in pregnant rats on the mineralocorticoid activity of the adrenals in their neonates

Exposure of pregnant rats to morphine, from day 11 to day 18 of gestation, was previously reported to induce both an adrenal atrophy and hypoactivity of the glucocorticoid function in newborns at term, but did not affect, in vitro, the responsiveness of those glands to adrenocorticotrophin hormone ( ACTH) concerning corticosterone release. Moreover, these effects were media ted by maternal hormones from the adrenal glands. In the present work, we i nvestigated the effects of a prenatal morphine exposure on the mineralocort icoid activity of the adrenals in neonates. The first aim of the present st udy was to determine in these newborns 1 degrees) the adrenal and plasma al dosterone concentrations at birth time and during the early postnatal perio d 2 degrees) the plasma levels of Na+ and K+ at birth time, 3 degrees) the in vitro responsiveness of the newborn adrenals to angiotensin II (A(II)) a nd ACTH. The second aim of our study was to investigate the mineralocortico id activity of the adrenals in newborns from adrenalectomized mothers treat ed with morphine during gestation. According to present data morphine given to intact mothers induced in newborns a severe adrenal atrophy but increas ed adrenal aldosterone content and plasma aldosterone level. However, prena tal morphine was unable to affect significantly Na+/K+ ratio in both mother s and newborns. In vitro, the adrenals of neonates from morphine-treated mo thers were unresponsive to A(II) and ACTH for promoting aldosterone release ; in contrast, aldosterone secretion was significantly stimulated by high p otassium levels (55 mEq). Maternal adrenalectomy performed one day before t he beginning of morphine treatment prevented morphine-induced adrenal atrop hy but was unable to affect significantly the adrenal mineralocorticoid fun ction of the offspring. Such data suggest that a prenatal morphine exposure stimulated both aldosterone synthesis and release in neonates. However, th is basal hyperfunction did not appear to be coupled with an enhanced adrena l responsivity to An: or ACTH. Prenatal morphine-induced hyperactivity of t he mineralocorticoid function of the newborn adrenals, which drastically co ntrast with hypoactivity of the glucocorticoid one, was independent of adre nal factors from maternal origin.