Relationship between Urinary Excretion Rate, Steady-State Plasma Levels and Diuretic Response of Furosemide in the Rat

Pharmacology ◽  
1979 ◽  
Vol 19 (6) ◽  
pp. 301-306 ◽  
Author(s):  
David E. Smith ◽  
Leslie Z. Benet
1986 ◽  
Vol 106 (7) ◽  
pp. 590-593
Author(s):  
JIABI ZHU ◽  
KAZUNORI KATAYAMA ◽  
MASAWO KAKEMI ◽  
TAMOTSU KOIZUMI

Nature ◽  
1963 ◽  
Vol 198 (4879) ◽  
pp. 450-453 ◽  
Author(s):  
T. CHULSKI ◽  
R. H. JOHNSON ◽  
C. A. SCHLAGEL ◽  
J. G. WAGNER

1997 ◽  
Vol 16 (11) ◽  
pp. 667-672 ◽  
Author(s):  
S. Halbach ◽  
L. Kremers ◽  
H. Willruth ◽  
A. Mehl ◽  
G. Welzl ◽  
...  

The number of amalgam-covered surfaces and the occlusal area of the fillings, the concentrations of total mercury in plasma, erythrocytes and urine, the urinary excretion rate, and the absorbed daily doses estimated by two separate methods from intra-oral Hg emission were determined in 29 volunteers with a low amalgam load. The transfer ofHg from the fillings via the oral cavity and blood to urinary excretion was evaluated by multiple correla tions between these variables. In addition, the combina tion of variables most representative of the entire compartmental transfer of amalgam Hg was determined. Urinary excretion (1), Hg concentration in plasma (2) and absorbed dose (3) were most closely correlated to each other, followed by correlations with the variables of the fillings (4). Correlation coefficients were 0.75 for variables 1 vs 2 and 2 vs 3, and 0.49 for variables 3 vs 4. It was concluded that variables 1-3 best reflected the transfer of mercury from amalgam fillings throughout the organism and that they were relatively insensitive to dietary mercury. The determination of total mercury in plasma and of its urinary excretion rate appears, under practical aspects, most suitable for the investigation of Hg uptake from amalgam.


1971 ◽  
Vol 40 (4) ◽  
pp. 351-364 ◽  
Author(s):  
A. Breckenridge ◽  
M. L'E. Orme ◽  
S. Thorgeirsson ◽  
D. S. Davies ◽  
R. V. Brooks

1. Administration of dichloralphenazone, a complex of chloral hydrate and phenazone (antipyrine) caused a fall in steady-state plasma warfarin concentration and loss of anticoagulant control in five subjects. 2. This effect of dichloralphenazone is due to stimulation of the drug-oxidizing enzymes of the liver endoplasmic reticulum by antipyrine, the non-hypnotic part of the complex. Administration of antipyrine caused a fall in steady-state plasma warfarin concentration in five subjects, a shortening of the plasma warfarin half-life, with increased urinary excretion of the metabolites of 14C-labelled warfarin in two subjects and increased urinary excretion of 6β-hydroxycortisol which is formed in the liver endoplasmic reticulum. 3. Administration of chloral hydrate, the hypnotic part of dichloralphenazone, caused no change in anticoagulant control but a fall in steady-state plasma warfarin concentration in five subjects. This is due to the accumulation of trichloroacetic acid which displaces warfarin from plasma protein binding sites. 4. Individual differences in the extent of enzyme induction have been shown to be related to the subjects' rates of drug oxidation. 5. In the rat administration of dichloralphenazone and antipyrine, but not chloral hydrate, caused shortening of pentobarbitone sleeping time and of the plasma [14C]pentobarbitone half-life, shortening of the zoxazolamine paralysis time and increase in the maximal velocity of N-demethylation of ethylmorphine.


Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3338-3343 ◽  
Author(s):  
Liomar A. A. Neves ◽  
Aleck F. Williams ◽  
David B. Averill ◽  
Carlos M. Ferrario ◽  
Michael P. Walkup ◽  
...  

Abstract The vasoactive effect of angiotensin (Ang)-(1–7) in mesenteric resistance arteries together with its plasma and kidney concentration and urinary excretion was assessed in pregnant and virgin rats. Mesenteric arteries (230–290 μm) were mounted in a pressurized myograph system and Ang-(1–7) concentration-dependent response curves (10−10–10−5m) were determined in arteries preconstricted with endothelin-1 (10−7m). The Ang-(1–7) response was investigated in vessels with and without pretreatment with the Ang-(1–7) antagonist [d-[Ala7]-Ang-(1–7)] (10−7m). Ang-(1–7) caused a significantly enhanced, concentration-dependent dilation of mesenteric vessels (EC50 = 2.7 nm) from pregnant compared with virgin female rats. d-[Ala7]-Ang-(1–7) eliminated the vasodilator effect of Ang-(1–7). There was no significant change in plasma concentration of Ang-(1–7) in pregnant animals. On the other hand, 24 h urinary excretion and kidney concentration of Ang-(1–7) were significantly higher in pregnant animals. The increased mesenteric dilation to Ang-(1–7) with enhanced kidney concentration and 24 h urinary excretion rate of Ang-(1–7) suggests an important role for this peptide in cardiovascular regulation during pregnancy.


1986 ◽  
Vol 251 (4) ◽  
pp. F581-F587 ◽  
Author(s):  
N. Perico ◽  
A. Benigni ◽  
C. Zoja ◽  
F. Delaini ◽  
G. Remuzzi

Animals and humans undergoing a chronic treatment with cyclosporin A (CyA) show a reduction in glomerular filtration rate (GFR). The cause of this abnormality has not been established. Since CyA interferes with arachidonic acid (AA) metabolism in various cells, we wished to determine whether alterations in renal AA metabolites contribute to deteriorating renal function in rats on CyA. We show that chronic CyA treatment induces a progressive increase in the renal synthesis of thromboxane (TX) A2. This is a selective abnormality in that CyA does not influence the renal synthesis of prostaglandin E2 (PGE2) and prostacyclin (PGI2). A significant negative correlation has been found between TXB2 urinary excretion rate and inulin clearance. No correlation has been observed between TXB2 excretion and p-aminohippuric acid clearance. The withdrawal of CyA is followed by a normalization of both TXB2 urinary excretion rate and GFR. The administration of a selective TXA2 inhibitor, UK-38,485, resulted in a significant reduction in urinary excretion of TXB2 accompanied by a significant increase in GFR. We conclude that chronic treatment with CyA in rats is associated with a selective increase in renal TXA2 synthesis and suggest that this abnormality may play a role in the reduction of GFR.


1989 ◽  
Vol 37 (2) ◽  
pp. 185-189 ◽  
Author(s):  
L. v. Bortel ◽  
R. Böhm ◽  
J. Mooij ◽  
P. Schiffers ◽  
K. H. Rahn

Guanidines 2 ◽  
1989 ◽  
pp. 137-146
Author(s):  
Yoshiyuki Takano ◽  
Fumitake Gejyo ◽  
Yoshio Shirokane ◽  
Moto-o Nakajima ◽  
Masaaki Arakawa

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