Drugs online research references
med.kitasato-u.ac.jp
This study examined whether the renal kallikrein-kinin system (KKS) is involved with furosemide-induced natriuresis in rats. Intravenous administration of furosemide (10 mg/kg) to anesthetized rats infused with physiological saline (saline) increased renal KK excretion as well as urine volume and urinary excretions of sodium, chloride and potassium. The change in the increase of renal KK excretion by furosemide at a dose of 1.0 mg/kg relative to the control was larger than that of urine volume. Pretreatment with a B2-receptor antagonist, 8-[3-[N-[(E)-3-(6-acetamidopyridin-3-yl)acryloylglycyl]-N-methylamino]-2,6-dichlorobenzyloxy]-2-methylquinoline (FR173657, 100 mg/kg), significantly inhibited the furosemide-induced natriuresis by 58.6%. The effect of FR173657 on the furosemide-induced natriuresis was also examined in hypotonic saline-loading rats. Similar to the saline-loading rats, urinary excretion of sodium collected during the first 8 h in metabolic cages significantly reduced by 22.4% when FR173657 (100 mg/kg) was given concurrently with furosemide (100 mg/kg) and hypotonic saline (5% of body wt.). These results indicate that furosemide increased renal KK excretion through a mechanism different from a washout mechanism and induced natriuresis partly through an augmentation of the renal KKS following the increase in renal KK excretion in both the saline- and hypotonic saline-loading rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11128035&dopt=Abstract
Endocrinology. 1980 Sep;107(3):771-3.
The effects of hemorrhage and sodium depletion on plasma concentrations of angiotensin II and [des-Asp1]angiotensin II in the rat.
Semple PF.
Plasma concentrations of angiotensin II (PAII) and [des-Asp1]angiotensin II (Pdes-Asp1-AII) were measured before and after hemorrhage and acute and chronic depletion of sodium. Graded hemorrhage increased PAII from 30 +/- 5 to 220 +/- 41 and 989 (526-1290) pmol/liter and Pdes-Asp1-AII from 47 +/- 11 to 216 +/- 72 and 532 +/- 178 pmol/liter. Furosemide increased PAII from 26 +/- 4 to 178 +/- 37 but did not change Pdes-Asp1-AII (31 +/- 3 to 31 +/- 4 pmol/liter). Deprivatin of dietary sodium increased PAII from 25+/- 6 to 136+/- 22 pmol/liter and Pdes-Asp1-AII from 41 +/- 4 to 71 +/- 15 pmol/liter. The ratio of PAII to Pdes-Asp1-AII was increased by all three stimuli (P < 0.05 to P < 0.001). Pdes-Asp1-AII II is unlikely to mediate the effects of hemorrhage and changes in sodium balance on aldosterone secretion in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7398582&dopt=Abstract
Prostaglandins. 1983 Jan;25(1):99-103.
Urinary prostaglandin and kallikrein excretion are not flow dependent in the rat.
Fejes-Toth G, Naray-Fejes-Toth A, Rigter B, Frolich JC.
To study the relationship between urine flow, urinary prostaglandin (PG) and kallikrein excretion in the rat high urine flow was induced in hydropenic Long-Evans rats by either hypotonic volume expansion or with mannitol or with furosemide. PGE2 excretion remained unchanged during hypotonic volume expansion (134.5 +/- 29.7 before and 153.0 +/- 48.9 pg/min after) while it decreased significantly with mannitol (from 166.3 +/- 32.4 to 45.2 +/- 8.2 pg/min, p less than 0.01) and with furosemide (from 170.0 +/- 20.4 to 29.5 +/- 5.3 pg/min, p less than 0.001). PGF2 alpha excretion rates were slightly reduced following all three interventions. Urinary kallikrein excretion remained unchanged in all three groups of animals. It is concluded that, in contrast to humans and dogs in the rat urine flow and urinary PG excretion are not interlinked.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6405455&dopt=Abstract
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