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Lei Yu, Haoran Wang, Xiaoxue Han, Honghui Liu, Dalong Zhu, Wenhuan Feng, Jinhui Wu and Yan Bi

lipid metabolism to avoid excessive hepatic lipid droplet deposition. However, destruction of the oxygen gradient by hypoxia accelerates hepatic steatosis ( Birchmeier 2016 , Kietzmann 2017 , 2019 ). Hypoxia-inducible transcription factors (HIFs) are

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Chisato Katoh, Tomohiro Osanai, Hirofumi Tomita and Ken Okumura

-constituting cells such as astrocytes. In this study, we investigated whether BNP expression is enhanced in cultured human astrocytoma cell line U373MG when exposed to hypoxia, and if so, what signaling pathway is involved. We also examined whether endogenous BNP

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Masami Hayashi, Masahiro Sakata, Takashi Takeda, Toshiya Yamamoto, Yoko Okamoto, Kenjiro Sawada, Akiko Kimura, Ryoko Minekawa, Masahiro Tahara, Keiichi Tasaka and Yuji Murata

response to oxygen deficiency in this organ. However, the precise mechanism regulating GLUT1 expression during placentation has not been fully clarified. Heterodimeric hypoxia-inducible factor-1 (HIF-1) is a transcriptional activator that mediates

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Charles A Ducsay and Dean A Myers

by hypoxia. As such, NO represents a potential mechanism for changes in steroidogenesis in response to hypoxia. This review will focus on the role of NO in the regulation of steroidogenesis and the potential interaction of NO production and hypoxia

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Daisuke Fujita, Akiko Tanabe, Tatsuharu Sekijima, Hekiko Soen, Keijirou Narahara, Yoshiki Yamashita, Yoshito Terai, Hideki Kamegai and Masahide Ohmichi

pregnancy. They demonstrated that the placenta develops in conditions of physiological hypoxia, in which the local oxygen concentration is as low as 1–2% during the first trimester. A significant increase was observed for placental PO 2 values measured at

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MARY L. FORSLING, D. L. INGRAM and M. W. STANIER

The level of antidiuretic hormone (ADH) in the plasma of pigs was studied during hypoxia, anaesthesia and a combination of the two conditions. Hypoxia, caused by making conscious pigs breathe nitrogen, elicited a rise in the level of ADH without change in plasma osmolality; the hypoxia was accompanied in some cases by a slight lowering of arterial pressure which quickly returned to its original level after the period of hypoxic breathing. Pentobarbitone anaesthesia had no significant effect on the level of ADH but halothane anaesthesia elicited a rise in ADH.

Transient high levels of ADH were seen in animals which were exposed to hypoxia during halothane or pentobarbitone anaesthesia. These high levels of ADH were sometimes, but not invariably, accompanied by a fall in arterial pressure. No consistent changes in plasma osmolality or haematocrit were associated with the raised plasma ADH.

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S. C. Griffen and H. Raff

ABSTRACT

The purpose of this study was to determine the effect of water restriction on the vasopressin response to hypoxia in conscious Long–Evans rats. Rats were prepared with chronic indwelling femoral artery and vein catheters 1 week before experimentation. At 24 h before the first blood sample, the supply of drinking water was maintained ad libitum (water replete) or removed (water deplete). At 24 h, a control blood sample was taken and then normoxia (21% O2) was maintained or hypoxia (10% O2) induced. Additional blood samples were taken at 1, 18 and 24 h. All blood samples (2·5 ml) were simultaneously replaced with donor blood to maintain isovolaemia. Hypoxia led to a very small and transient increase in vasopressin in the water-replete rats. The combination of hypoxia and water restriction led to a greatly augmented vasopressin response at 1 h (60 ± 16 pmol/l); this response was also not sustained. Additional non-cannulated rats were exposed to 24 h of normoxia or hypoxia with or without water available ad libitum and posterior pituitaries were collected after decapitation for measurement of vasopressin content. Water restriction, hypoxia and water restriction plus hypoxia all led to decreased pituitary vasopressin content. We conclude that the vasopressin response to hypoxia in conscious rats is small and transient, and that concomitant water restriction augments the vasopressin response to acute but not chronic hypoxia.

Journal of Endocrinology (1990) 125, 61–66

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J. R. CLAYBAUGH, J. E. HANSEN and D. B. WOZNIAK

SUMMARY

Eight men, 19-35 years of age, breathed 20·9% (normal oxygen), 13·9% (mild hypoxia) or 11·1% (severe hypoxia) oxygen in nitrogen gas mixtures during three 20 min periods, which were separated by 1 h recovery periods. The order in which the gas mixtures were breathed was random. The partial pressure of oxygen decreased from a mean of 93·5 during exposure to normal oxygen to 53·9 and 36·7 mmHg during mild and severe hypoxia respectively. There were corresponding decreases in haemoglobin saturation. The partial pressure of carbon dioxide was lower and the pH higher during severe hypoxia than during exposure to normal oxygen. There were no changes in the plasma osmolality or in the concentrations of sodium or potassium in the plasma. There was a tendency for both the renin activity and the concentration of aldosterone in the plasma to decrease progressively as the percentage of oxygen breathed decreased. Unlike severe hypoxia, mild hypoxia suppressed the concentration of antidiuretic hormone (ADH) in the plasma of all subjects by about 59%; during severe hypoxia the reduction was not significant, being only about 33%. These data are consistent with the suggestion that the effect of hypoxia on the release of ADH is dependent on the level of hypoxia.

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PS Leung, SY Lam and ML Fung

In the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT(1) and AT(2), in the carotid body. The mRNA expression for subtypes of the AT(1) receptor, AT(1a) and AT(1b), was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT(1) receptor, an immunohistochemical study was performed. The results showed that AT(1) receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT(1) receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT(1) receptors in the rat carotid body. The upregulation of the expression also enhances AT(1) receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.

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M Tucci, K Nygard, BV Tanswell, HW Farber, DJ Hill and VK Han

Endothelial cells (EC) are hypoxia-tolerant and their capacity to proliferate in low oxygen tension is essential to maintain vascular endothelium integrity. The present study addresses whether hypoxia alters the expression of insulin-like growth factor (IGF) and IGF binding protein (IGFBP) genes in bovine aortic EC (BAEC) and bovine pulmonary artery EC (BPAEC). EC were cultured in normoxic (21%) conditions and exposed to 0% oxygen for 24, 48, or 72 h; some cells were reoxygenated by exposure to 21% oxygen for 24 or 48 h following hypoxia. IGF-I peptide and mRNA levels were very low in both cell types, and decreased further with exposure to hypoxia. Ligand blotting showed that both cell types synthesized 24 kDa (IGFBP-4), 30 kDa (IGFBP-5 and/or IGFBP-6), 43 kDa and 48 kDa IGFBPs (IGFBP-3 glycosylation variants). IGFBP-4 was the predominant IGFBP expressed by both cell types and did not change with exposure to hypoxia. Hypoxia caused a significant increase in IGFBP-3 secretion in BPAEC but not in BAEC. IGFBP-3 stable mRNA levels in BPAEC were increased correspondingly. IGFBP-5 was expressed only in BAEC and decreased with exposure to hypoxia. IGFBP-6 mRNA expression was low and increased in both cell types with exposure to hypoxia. These results demonstrate that EC IGFBP baseline expression as well as its expression in hypoxia vary in different vascular beds and suggest that the IGFBPs may be the dominant paracrine regulators of proliferation of EC as well as maintenance of endothelium integrity during hypoxia.