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)

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.
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PMID:Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression. 91 12

Early alterations in fluid, electrolytes, and their regulating hormones were investigated in men exposed to 6,000 m simulated altitude (2 h-ascent, 2 h-sojourn, 2 h-return). Hematocrit and serum protein rose with elevated serum osmolality and reduced urine flow upon arrival at 6,000 m, suggesting decreased plasma volume probably due to hypotonic fluid shift to intracellular spaces. Serum K declined reflecting respiratory alkalosis. The exposure raised plasma antidiuretic hormone (ADH), plasma renin activity (PRA), serum cortisol and aldosterone. Increases both in ADH and aldosterone showed close correlations with that in cortisol, suggesting that ADH may be elevated by hypoxic stress in addition to elevated serum osmolality and decreased plasma volume, and that increased secretion of adrenocorticotropin may be the main cause of increased aldosterone, though PRA involvement cannot be excluded. These rises in ADH and aldosterone may act to retain body water, and the latter may exaggerate alkalosis; thus, these hormonal changes may be related to acute mountain sickness.
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PMID:Hormonal disturbances of fluid-electrolyte metabolism under altitude exposure in man. 637 81

Sudden ascent to high altitudes beyond 2,438 m can cause life-threatening complications such as acute mountain sickness and high altitude cerebral and pulmonary oedema. We present a case of pituitary apoplexy in a young man who ascended to high altitude gradually, after proper acclimatisation. He developed headache, nausea, vomiting and persistent hypotension. Magnetic resonance imaging revealed an enlarged pituitary gland with haemorrhage. His hormonal estimation showed acute adrenal insufficiency due to corticotropin deficiency. The patient responded well to conservative medical management with hormonal replacement therapy. This is most likely the first reported case of high altitude-induced pituitary apoplexy in the literature.
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PMID:High altitude-induced pituitary apoplexy. 2294 Nov 36

We have shown that hypoxia reduces plasma insulin, which correlates with corticotropin-releasing hormone (CRH) receptor 1 (CRHR1) in rats, but the mechanism remains unclear. Here, we report that hypobaric hypoxia at an altitude of 5,000 m for 8 h enhances rat plasma CRH, corticosterone, and glucose levels, whereas the plasma insulin and pancreatic ATP/ADP ratio is reduced. In islets cultured under normoxia, CRH stimulated insulin release in a glucose- and CRH-level-dependent manner by activating CRHR1 and thus the cAMP-dependent protein kinase pathway and calcium influx through L-type channels. In islets cultured under hypoxia, however, the insulinotropic effect of CRH was inactivated due to reduced ATP and cAMP and coincident loss of intracellular calcium oscillations. Serum and glucocorticoid-inducible kinase 1 (SGK1) also played an inhibitory role. In human volunteers rapidly ascended to 3,860 m, plasma CRH and glucose levels increased without a detectable change in plasma insulin. By contrast, volunteers with acute mountain sickness (AMS) exhibited a marked decrease in HOMA insulin sensitivity (HOMA-IS) and enhanced plasma CRH. In conclusion, hypoxia may attenuate the CRH-insulinotropic effect by reducing cellular ATP/ADP ratio, cAMP and calcium influx, and upregulated SGK1. Hypoxia may not affect HOMA-IS in healthy volunteers but reduces it in AMS volunteers.
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PMID:Inactivation of corticotropin-releasing hormone-induced insulinotropic role by high-altitude hypoxia. 2527 97