Studies were performed on the reactivity of the hypothalamopituitary-adrenocortical axis of intact, gonadectomized, and testosterone-or estradiol-replaced rats to standard ether stress. Plasma ACTH and corticosterone (B) levels, anterior pituitary ACTH, and adrenal B content were estimated 20 and 40 min after stress application and in unstressed animals. Ether stress resulted in an increase in plasma ACTH and B levels and in adrenal B content while pituitary ACTH content was notably lower when compared with unstressed rats. The response was markedly higher in female than in male rats. After orchiectomy and testosterone replacement, plasma ACTH and B responses to ether stress were similar to those observed in intact male rats. On the other hand, ovariectomized females responded to ether stress like intact males, while after estradiol replacement the pattern of plasma ACTH and B concentration and adrenal B content was similar to that in intact female rats. Thus, the higher responsiveness of the pituitary-adrenal cortex axis of female rats to ether stress depends on stimulatory or facilitatory effect of estradiol.

The morphologic changes evoked in the adrenal glands of male and female hamsters by gonadectomy (15 weeks) and gonadal-hormone replacement (single s.c. injection of 5 mg/l00 g b.w. testosterone or 0.5 mg/l00 g b.w. estradiol, 2 weeks before the sacrifice) were investigated by morphometric techniques and correlated with the functional alterations of the hypothalamopituitary-adrenal axis. Our findings evidenced a stimulatory role of androgens and a moderate inhibitory one of estrogens on the growth and steroidogenic capacity of the adrenal glands in male and female hamsters, respectively. Moreover, they suggest that these adrenal effects of gonadal hormones are, at least partly, independent of alterations in the pituitary ACTH release.

The development of the human fetal adrenals starts in the 6th week gestational age and adrenal C19 steroid production becomes of major importance for the maintenance of the pregnancy. Therefore, in the present study, human fetal adrenals at 6 weeks of gestational age were immunostained for 17 alpha-hydroxylase, the key enzyme for the production of C19-steroids. In parallel, chromaffin cells were characterized by immunohistochemical staining for chromogranin A, the major soluble protein in adrenal chromaffin granules. Large 17 alpha-hydroxylase-immunoreactive cells were found in the center of the adrenal anlagen during the 6th week of gestation. At the same developmental stage, chromaffin cells with a neuronal-like appearance occurred in the paraortic area and started to invade the adrenal primordium. Our results show that, even at week 6 gestational age, when chromaffin cells start to enter the adrenal anlagen, human adrenals already contain differentiated, 17 alpha-hydroxylase immunoreactive cortical cells which were located to the center of the primordium.

Plasma ACTH and corticosterone (B) concentration, ACTH content in the anterior pituitary gland and B content in the adrenals were measured in intact, gonadectomised and testosterone or estradiol replaced rats.Plasma ACTH and B levels and adrenal B content were higher in female than male rats. Neither orchiectomy nor testosterone replacement had an effect on plasma ACTH and B concentration. Orchiectomy did not affect adrenal B content and decreased pituitary ACTH while testosterone significantly lowered ACTH and B content in studied glands. On the other hand ovariectomy did not change pituitary ACTH and adrenal B content and notably lowered concentrations of these hormones in the blood. Estradiol replacement resulted in an increase in plasma ACTH and B concentrations, an effect accompanied by a marked drop in pituitary ACTH and an increase in adrenal B.These findings indicate the distinct sex differences in basal plasma ACTH and B concentrations with higher values in female rats, an effect dependent on the stimulatory action of estradiol on pituitary-adrenocortical axis.

Acute ANF bolus administration (40 micrograms.kg-1) did not affect secretory activity and morphology of rat Leydig cells. Prolonged (7-day) ANF infusion (20 micrograms.kg-1.h-1), on the contrary, elevated both basal and hCG-stimulated testosterone blood concentration, and caused a notable hypertrophy of rat Leydig cells. Leydig-cell hypertrophy was due to increases in the volume of all the organelles involved in cholesterol and testosterone synthesis (i.e. mitochondria, smooth endoplasmic reticulum and peroxisomes). These findings suggest that ANF, when chronically administered, is able to stimulate the growth and steroidogenic capacity of rat Leydig cells.