The effects of electrical stimulation of the brain on the ovarian venous plasma concentrations of estradiol (E2) and progesterone (P) were investigated in female rats hypophysectomized and adrenalectomized at 1000 h on the day of proestrus. Stimulation was applied during the proestrous critical period under pentobarbital anesthesia, and contralateral ovarian venous blood was collected from 105-120 min after the stimulation. E2 and P concentrations, estimated by RIA, were significantly increased by stimulation of the medial basal prechiasmatic area (PVA), ventromedial hypothalamus, and areas in the mesencephalon and decreased by stimulation of the dorsal hippocampus, lateral amygdala, and mesencephalic areas. Ovarian blood flow was not affected by these stimulations. Ovarian nervotomy in the proestrous rats abolished E2 secretion induced by PVA stimulation. In intact proestrous rats, electrochemical stimulation of the PVA but not the preoptic suprachiasmatic area increased E2 and P concentrations, although stimulation of both areas commonly potentiated gonadotropin secretion. Present findings suggest that the efferent neural system from the brain to the ovaries is supplementary to the brain-pituitaryovarian hormonal mechanisms in the regulation of ovarian steroid secretion, and the system may be required for the adjustment of ovarian responsiveness and sensitivity to gonadotropins. In addition, evidence for neural feedback on basal FSH secretion in the ovarian-denervated proestrous rats is presented in this study. {Endocrinology 109: 136, 1981) I T HAS been demonstrated in rats that the cyclic alteration of ovarian steroid biosynthesis (1) and secretion (2, 3) are temporally related to the cyclic changes of gonadotropin secretion throughout the estrous cycle. The administration of gonadotropins to cyclic rats increased or decreased ovarian biosynthetic activity (1), and the effects were altered qualitatively and quantitatively during the estrous cycle (1, 4). However, it is still obscure whether the cyclic changes in ovarian steroid synthesis and release depend only upon gonadotropin secretion. Stimulation of the dorsal hippocampus (d-HPC) during the estrous cycle changed steroid biosynthetic activity without affecting gonadotropin secretion (4) or pituitary stalk blood LHRH concentration (5). More recently, d-HPC stimulation was shown to induce alterations in ovarian estrogen and progestin biosyntheses in pituitary-lesioned rabbits pretreated with 20a-hydroxyprogesterone (6). The above findings indicate the existence of other mechanisms besides the gonadotropin regulation of ovarian steroid synthesis and release.Recently, adrenergic and cholinergic projections to the

No abstract

No abstract

No abstract

The plasma corticosterone concentration and incorporation of 14C-1-acetate into adrenocortical hormones were measured in male rats exposed to hypoxia (12.5% O2 in N2 balance) for periods of 30 min--14 days. Hypoxia significantly increased the weight of the adrenal and pituitary glands in early stages of exposure. However, weight returned to the control level on the 14th day of exposure. Hypoxia consistently decreased the weight of the thymus. Hypoxia elevated the plasma corticosterone concentration in the early stages of exposure. However, the elevated corticosterone level gradually decreased by the 7th day. The corticosterone level at this stage was lower than in the control. The corticosterone concentration returned to the control level on the 14th day. Hypoxia significantly facilitated incorporation of 14C-1-acetate into corticosterone and cortisol in the adrenal homogenate. The elevated incorporation was maintained until the 7th day and gradually decreased to the control level there after. Body weight was decreased by hypoxia (12 gram in 24 hours). On the 5th day, the weight returned to the control level. Hematocrit increased gradually during 14 days of hypoxia exposure. These results suggest that pituitary-adrenal function is greatly facilitated by 1-6 hours of hypoxia exposure, and hypoxia acclimatization is accomplished humorally within 14 days of exposure in rats.