Abstract |
Injections of furosemide at a dose of 0.3 micromol per 100 g body weight or 1-deamino-arginine-vasotocin (1dAVT) at a dose of 0.05 nmol per 100 g body weight induced nearly equal increase in urinary sodium excretion: up to 406 +/- 20 and 405 +/- 23 micromol/2 h, respectively. Increase in urinary sodium excretion after injection of 1d-AVT was followed by enhancement of solute free water reabsorption from -0.51 +/- 0.05 to -2.75 +/- 0.11 ml/2 h (p < 0.05). On the contrary, furosemide injection induced a significant decrease in solute free water reabsorption to -0.19 +/- 0.06 ml/2 h (p < 0.05) and led to the appearance of solute free water in urine during peak of diuretic reaction. These data for the first time show that furosemide not only decreases sodium reabsorption, but also blocks some componentin molecular mechanism of vasopressin-dependent increase of the osmotic permeability of water.
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Authors | A V Kutina, Iu V Natochin |
Journal | Eksperimental'naia i klinicheskaia farmakologiia
(Eksp Klin Farmakol)
Vol. 73
Issue 5
Pg. 19-22
(May 2010)
ISSN: 0869-2092 [Print] Russia (Federation) |
PMID | 20597365
(Publication Type: Comparative Study, English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Diuretics
- vasotocin, 1-deamino-arginine-
- Water
- Furosemide
- Sodium
- Vasotocin
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Topics |
- Animals
- Diuretics
(pharmacology)
- Female
- Furosemide
(pharmacology)
- Kidney Tubules
(metabolism)
- Natriuresis
(drug effects)
- Osmosis
- Permeability
- Rats
- Rats, Wistar
- Sodium
(urine)
- Vasotocin
(analogs & derivatives, pharmacology)
- Water
(metabolism)
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