Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biologically active plasma free cortisol increases markedly in pregnancy. In this investigation the free cortisol index (FFI) in the plasma of pregnant and nonpregnant women was measured by a charcoal adsorption technique. The circadian FFI patterns were virtually identical in the two groups, but in gravid women there was a substantial and sustained elevation of the FFI. Sequential studies during gestation and post partum revealed increasing responsiveness of the maternal adrenal glands to adrenocorticotropic hormone (ACTH) and decreasing suppressibility of the FFI by dexamethasone as pregnancy advanced. Persistence of normal circadian rhythmicity in spite of a continuously elevated FFI and resistance to dexamethasone suppression suggest control of cortisol secretion by normal regulatory mechanisms in pregnancy with resetting of the maternal feedback mechanisms to higher levels. This resetting and the lack of manifestations of cortisol excess in pregnancy might result from tissue refractoriness to cortisol. Elevated free cortisol would be needed to maintain homeostasis. The necessary increase in the production of cortisol could be facilitated by an enhanced responsiveness of the maternal adrenal glands to ACTH.
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PMID:Elevated free cortisol index in pregnancy: possible regulatory mechanisms. 625 37

Fatal familial insomnia is a prion disease in which a selective thalamic degeneration leads to total sleep deprivation, hypertension, dysautonomia, adrenal overactivity, and impaired motor functions. With patients under continuous recumbency and polysomnographic control, we assessed the changes in the 24-hour patterns of blood pressure, heart rate, plasma catecholamines, corticotropin, and serum cortisol in three patients at different stages of the disease. Six healthy volunteers were used as control subjects. A dominant 24-hour component was detected at rhythm analysis of all variables, both in patients and control subjects. In the patients, the amplitudes gradually decreased as the disease progressed, leading to the obliteration of any significant dirunal variation only in the preterminal stage. A shift in phase corresponded to the loss of the nocturnal fall in blood pressure in an early stage of the disease, when nocturnal bradycardia was still preserved. Plasma cortisol was high and became increasingly elevated, whereas corticotropin remained within normal levels; abnormal nocturnal peaks appeared in their circadian patterns. The disrupted patterns of cortisol and blood pressure preceded the development of hypertension and severe dysautonomia, which in turn were paralleled by increasing catecholamine and heart rate levels. Our data demonstrate that in patients with fatal familial insomnia the changes detectable in the rhythmic component of diurnal blood pressure variability result in a pattern of secondary hypertension. Disturbances in thalamic, pituitary-adrenal, and autonomic functions seem to be involved in mediating these changes.
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PMID:Diurnal blood pressure variation and hormonal correlates in fatal familial insomnia. 817 63