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1 d-type (WT) mice while maintaining a similar plasma osmolality.
2 ta mRNA correlated inversely with changes in plasma osmolality.
3 onse to angiotensin II; and (c) reduction in plasma osmolality.
4 ipheral circulation in response to increased plasma osmolality.
5 ality failed to decrease at the same rate as plasma osmolality.
6 ncomitant with increases in fluid intake and plasma osmolality.
7 travenous infusion of HYPER saline increased plasma osmolality (294 +/- 3 to 316 +/- 5 mOsm kg(-1) H2
8 induced drinking, vasopressin (AVP) release, plasma osmolality and c-fos expression in the brain of c
9 Loads of 900 and 1200 mOsm/kg both increased plasma osmolality and sodium concentration by 15 min aft
10 smotic stimulus, determined by assessment of plasma osmolality and sodium content, SON neurons exhibi
13 ration, which in turn influence the osmotic (plasma osmolality) and blood volume-dependent compensato
15 ydration status, including hematocrit, total plasma osmolality, and plasma protein concentration, fai
16 s generally accepted that dialysis may lower plasma osmolality at a faster rate than changes in ocula
17 rea bath decreased plasma urea by 21 mM, and plasma osmolality by 22 mosmol/kg H2O, and increased bra
19 decrease in urinary osmolality, and rise in plasma osmolality in the OPC 31260-treated CHF rats as c
21 dration-induced anorexia in which increasing plasma osmolality leads to a centrally generated reducti
25 ting these results with ongoing behavior and plasma osmolality points to the existence of brain netwo
26 l plasma sodium (WD(5)), the substitution of plasma osmolality (Posm) for sodium (WD(6)), and actual
27 hat individuals classified as DE have higher plasma osmolality (Posm), indicating suboptimal hydratio
30 , which produced a physiological increase in plasma osmolality to 299 +/- 1 mosmol (kg water)(-1), el
35 ared different equations used for predicting plasma osmolality when its direct measurement was not pr
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