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1 hetic nervous system responses to body fluid hyperosmolality.
2 bits later stages of apoptosis during severe hyperosmolality.
3 tic DNA damage within 48 h after exposure to hyperosmolality.
4 different degrees at identical strengths of hyperosmolality.
5 hyperinsulinemia, hypertriglyceridemia, and hyperosmolality.
6 ers measured indicated cell death because of hyperosmolality.
7 ed for approximately 18 h following onset of hyperosmolality.
8 ibited even in the presence of physiological hyperosmolality.
9 ere exposed to different degrees of hypo- or hyperosmolality 15 min prior to and during a 15-min hypo
10 to determine if sympathoexcitatory levels of hyperosmolality activate specifically those OVLT neurone
12 tal techniques, this study demonstrates that hyperosmolality and lactate are the major vasoactive com
13 ed a urinary concentrating defect with serum hyperosmolality and low urine osmolality that was not in
14 enal medulla from the deleterious effects of hyperosmolality and regulates the urinary concentration
15 common but also in distinct pathways during hyperosmolality and that their increased abundance contr
17 onstrated that at 24 and 48 h after onset of hyperosmolality, but not in isosmotic controls, growth a
18 ehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or in
27 results provide direct evidence that plasma hyperosmolality exerts a central modulatory effect gover
31 ly unknown plasma membrane protein and forms hyperosmolality-gated calcium-permeable channels, reveal
33 either induced or repressed in expression by hyperosmolality in a time- and osmolality-dependent fash
34 ed acutely by arginine vasopressin (AVP) and hyperosmolality in rat terminal inner medullary collecti
38 (HNa) is most potent in this regard, whereas hyperosmolality in the form of elevated urea (HU) does n
40 AQP1 protein, but not mRNA, was induced by hyperosmolality in vitro, suggesting post-transcriptiona
45 ously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory
47 ensing Ca(2+) channels serve as osmosensors, hyperosmolality-induced [Ca(2+)]i increases have been wi
50 More recently, it has been recognized that hyperosmolality is capable of also provoking a significa
51 accumulate organic osmolytes when exposed to hyperosmolality, most often in the form of high salt or
55 differential signaling to SCT in settings of hyperosmolality or food intake, modulated by differences
57 creased in cirrhosis and in cells exposed to hyperosmolality, suggesting that these miRs mediate osmo
58 l AQP and NKCC2, studies were performed with hyperosmolality that was induced by 0.5% NaCl in drinkin
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