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1 synthetase is transcriptionally regulated by hyperosmolality.
2 hetic nervous system responses to body fluid hyperosmolality.
3 bits later stages of apoptosis during severe hyperosmolality.
4 tic DNA damage within 48 h after exposure to hyperosmolality.
5  different degrees at identical strengths of hyperosmolality.
6  hyperinsulinemia, hypertriglyceridemia, and hyperosmolality.
7 ers measured indicated cell death because of hyperosmolality.
8 ed for approximately 18 h following onset of hyperosmolality.
9 ibited even in the presence of physiological hyperosmolality.
10 ere exposed to different degrees of hypo- or hyperosmolality 15 min prior to and during a 15-min hypo
11 to determine if sympathoexcitatory levels of hyperosmolality activate specifically those OVLT neurone
12                                              Hyperosmolality (adding 150 mM NaCl) strongly induces ph
13 tal techniques, this study demonstrates that hyperosmolality and lactate are the major vasoactive com
14 ed a urinary concentrating defect with serum hyperosmolality and low urine osmolality that was not in
15 enal medulla from the deleterious effects of hyperosmolality and regulates the urinary concentration
16  common but also in distinct pathways during hyperosmolality and that their increased abundance contr
17                             It is known that hyperosmolality and various other stimuli trigger increa
18 onstrated that at 24 and 48 h after onset of hyperosmolality, but not in isosmotic controls, growth a
19 ehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or in
20                                       Plasma hyperosmolality delayed the mean body temperature onset
21            The main findings are that plasma hyperosmolality delays the increase in skin sympathetic
22                                       Plasma hyperosmolality delays the onset for sweat production an
23                            In humans, plasma hyperosmolality delays the onset of sweating and cutaneo
24            These results suggest that plasma hyperosmolality delays the onset threshold for sweating
25                                              Hyperosmolality due to high dietary salt intake has been
26 nal tubular cells adjust to the intraluminal hyperosmolality during urinary concentration.
27                This study examined if plasma hyperosmolality exerts a central and/or peripheral modul
28  results provide direct evidence that plasma hyperosmolality exerts a central modulatory effect gover
29 s in humans; however, the mechanism by which hyperosmolality exerts this effect remains unknown.
30               However, it remains unknown if hyperosmolality exerts this effect through a central (i.
31                           Here we describe a hyperosmolality-gated calcium-permeable channel and its
32 ly unknown plasma membrane protein and forms hyperosmolality-gated calcium-permeable channels, reveal
33                                   Body fluid hyperosmolality has long been known to elicit homeostati
34 either induced or repressed in expression by hyperosmolality in a time- and osmolality-dependent fash
35 CA1 was discovered that functions in sensing hyperosmolality in Arabidopsis Here, we report the cryo-
36 ed acutely by arginine vasopressin (AVP) and hyperosmolality in rat terminal inner medullary collecti
37               Gadd45 proteins are induced by hyperosmolality in renal inner medullary (IM) cells, but
38             For investigation of the role of hyperosmolality in the absence of hyperglycemia on the r
39                                              Hyperosmolality in the form of elevated NaCl (HNa) is mo
40 (HNa) is most potent in this regard, whereas hyperosmolality in the form of elevated urea (HU) does n
41                                          The hyperosmolality in the renal medullary interstitium is o
42   AQP1 protein, but not mRNA, was induced by hyperosmolality in vitro, suggesting post-transcriptiona
43 lary collecting duct cells were sensitive to hyperosmolality in vitro.
44              This study examined the role of hyperosmolality in vivo to modulate aquaporin 2 (AQP2) a
45                                              Hyperosmolality increased luciferase activity equally (5
46                                              Hyperosmolality increases AR transcription through an os
47 ously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory
48  a much lesser extent than expected from the hyperosmolality induced by acute osmotic stimuli.
49 ), which is much less than expected from the hyperosmolality induced by saltloading.
50       In primary NFAT5 deficient IMCD cells, hyperosmolality induced changes in gene expression were
51                          The majority of the hyperosmolality induced transcripts in primary IMCD cult
52                  One of the mutants, reduced hyperosmolality-induced [Ca(2+)]i increase 1 (osca1), di
53 ensing Ca(2+) channels serve as osmosensors, hyperosmolality-induced [Ca(2+)]i increases have been wi
54 solated Arabidopsis mutants that exhibit low hyperosmolality-induced [Ca(2+)]i increases.
55                                              Hyperosmolality-induced increases in action potential fi
56                             We conclude that hyperosmolality induces p38 and SAPK/JNK cascades in mam
57   More recently, it has been recognized that hyperosmolality is capable of also provoking a significa
58 of arginine vasopressin (AVP) in response to hyperosmolality is critical.
59 tear quantity or quality, is associated with hyperosmolality, making electrolyte composition an impor
60 accumulate organic osmolytes when exposed to hyperosmolality, most often in the form of high salt or
61                Hyperglycemia with associated hyperosmolality occurred in diabetic BB rats (BBDM).
62                                        While hyperosmolality of the kidney medulla is essential for u
63 the effects of Gadd45 super-induction during hyperosmolality on G(2)/M arrest and apoptosis.
64 differential signaling to SCT in settings of hyperosmolality or food intake, modulated by differences
65                               In conclusion, hyperosmolality, secondary to either glucose or NaCl, up
66 , leading to a model of how it could mediate hyperosmolality sensing and transport pathway gating.
67  understand the structural basis of proposed hyperosmolality sensing in a staple crop plant, extend o
68 creased in cirrhosis and in cells exposed to hyperosmolality, suggesting that these miRs mediate osmo
69 l AQP and NKCC2, studies were performed with hyperosmolality that was induced by 0.5% NaCl in drinkin
70                                              Hyperosmolality that was induced by NaCl increased signi
71 ulating water balance and is released during hyperosmolality to limit renal water excretion.