PubMed · 13105884
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G DELL'ACQUA. 1953. [Adrenal function tests].. https://pubmed.ncbi.nlm.nih.gov/13105884/
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Administration (ip) of an opioid peptide, beta-endorphin (beta-EP) (0.1, 0.5, or 1 microg beta-EP/day/lizard for 30 days) during seasonal recrudescence phase of the ovarian cycle inhibited ovarian recrudescence as shown by the absence of vitellogenic follicles in the ovary in contrast to their presence in treatment controls in the lizard Mabuya carinata. In the germinal bed, treatment of 0.1 microg beta-EP did not affect primordial follicles, whereas their mean number was significantly lower in lizards treated with 0.5 or 1 microg beta-EP compared to those of treatment controls. There was also suppression of oviductal development as shown by a significantly lower relative weight of the oviduct and regressed oviductal glands in lizards treated with all the dosages of beta-EP compared to treatment controls. In another experiment, administration of FSH (10 IU FSH/alternate day/lizard for 30 days) during the regression phase of the ovarian cycle induced development of vitellogenic follicles, whereas the treatment controls showed only previtellogenic follicles. In addition, there was a significant increase in the ovarian and oviductal weights compared to initial and treatment controls. However, simultaneous administration of similar dosage of FSH and beta-EP (0.5 microg/day/lizard) did not induce ovarian recrudescence as shown by the absence of vitellogenic follicles in the ovary and significantly lower weight of the ovary and the oviduct and the mean number of oogonia, oocytes, and primordial follicles compared to those of FSH-treated lizards. The results indicate that beta-EP inhibits seasonal as well as FSH-induced ovarian recrudescence. Inhibitory effect of beta-EP on follicular development despite FSH administration implies its effect at the ovarian level in M. carinata. While adversely affecting the ovarian follicular development, beta-EP did not affect the adrenal gland as there was no significant variation in the mean nuclear diameter of the adrenocortical cells of treatment controls and beta-EP-treated lizards. Furthermore, administration of beta-EP caused a significant decrease in the mean number of islands of white pulp of the spleen indicating its adverse effect on immunity.
The present study tested the hypothesis that, in normal male rats, chronic changes in salt intake alter the levels of tyrosine hydroxylase and the norepinephrine transporter in sympathetic ganglia. Increasing dietary salt (from 0.02% to 1%, 4% or 8% NaCl in rat chow) decreased (p<0.05) the mRNA levels of tyrosine hydroxylase and the norepinephrine transporter in the adrenal gland, superior cervical ganglia and celiac ganglia. In addition, tyrosine hydroxylase and norepinephrine transporter protein levels were decreased (p<0.05) in the adrenal gland. To test the hypothesis that NaCl acts directly on postganglionic neurons to suppress the expression of these proteins, it was determined if increases in NaCl concentrations, of a magnitude achieved during increases in dietary salt in vivo, suppress expression of tyrosine hydroxylase and the norepinephrine transporter in cultured sympathetic neurons in vitro. Increased dietary salt increased plasma NaCl concentrations each by up to 4-6 mEq l(-1) (p<0.05), with the greatest increases occurring at night when the rats consume most of their food. In addition, NaCl added to cultured neurons decreased tyrosine hydroxylase and norepinephrine transporter protein and mRNA levels, and norepinephrine uptake; however, the NaCl concentration increases required were 15-30 mEq l(-1). These data suggest that increased dietary salt can influence the activity of the sympathetic nervous system by suppressing the levels of tyrosine hydroxylase and the norepinephrine transporter. While increased NaCl levels can act directly on neurons to suppress these proteins, this action may occur in vivo only in severe pathophysiological states, but not during increases in dietary salt without the synergistic effect of other factors.
The development of diseases in later life, such as diabetes type II, hypertension and cardiovascular disease, is linked to abnormal intrauterine conditions that reduce birth weight. Obviously, fetal development can be disturbed so profoundly, that fetal programming is changed permanently. We have examined the effects of hypoxia, or more precisely hypoxemia, on the fetal hypothalamic-pituitary-adrenal (HPA) axis and lungs using molecular biology techniques in order to elucidate the underlying mechanisms. Chronically catheterized fetal sheep were subjected to a hypoxemia (48 h) without change in arterial pH or paCO2. Major changes occurred, although the degree of hypoxemia was just moderate. There was a transient increase in the fetal plasma ACTH-concentrations with an upregulation of the cortisol-concentrations, which was more pronounced in the older, hypoxemic fetuses (134-136 days of gestation) than in the younger, hypoxemic animals (126-130 days of gestation; term is 145 days). There was an unique, differential regulation for pro-opiomelanocortin messenger RNA (mRNA), the precursor molecule of e.g. ACTH, in the pars distalis and pars intermedia of the pituitary gland. This finding supported the increased bioactivity besides the increased concentrations for ACTH. Simultaneously, there was an increase in the mRNAs of the ACTH-receptor and of the steroid-synthesizing enzymes in the fetal adrenal gland of the older, hypoxemic fetuses. No changes in the fetal plasma androstenedione-concentrations were observed. Clearly, there was a selective increase of the cortisol-synthesis. Growth and maturation of the fetal lung might also have been affected, because of the increase in surfactant-protein A mRNA in the older, hypoxemic animals and the decrease in the insulin-like growth factor-I and its binding protein-5 mRNA in the younger, hypoxemic fetuses. In summary, even a moderate degree of hypoxemia was shown to affect the different levels of fetal organism profoundly, offering a pathophysiological basis for changes in fetal development.