The Effect of Intravenous Infusions on the Urinary Excretion of Sodium

Physiology ◽  
2015 ◽  
pp. 86-98
Author(s):  
H. E. de Wardener
Keyword(s):  
Urinary Excretion ◽  
Intravenous Infusions

EFFECTS OF ANGIOTENSIN INFUSIONS ON URINARY EXCRETION OF COMPOUND III AND SUBSTANCES OTHER THAN ALDOSTERONE

1962 ◽  
Vol 40 (1) ◽  
pp. 727-738 ◽  
Author(s):  
Wojciech Nowaczynski ◽  
Erich Koiw ◽  
Pierre Biron ◽  
Michel Chrétien ◽  
Jacques Genest
Keyword(s):  
Angiotensin Ii ◽  
Urinary Excretion ◽  
Ultraviolet Light ◽  
Intravenous Infusions ◽  
Human Volunteers

Intravenous infusions of synthetic angiotensin II in human volunteers resulted in the increase of the urinary excretion of at least three ultraviolet light absorbing substances referred to as compounds III, IX, and X. This was concomitant with the increase of the urinary aldosterone excretion.Compound III has been partially described before; this is extended. A brief characterization of compounds IX and X is included (see Appendix).

EFFECTS OF ANGIOTENSIN INFUSIONS ON URINARY EXCRETION OF COMPOUND III AND SUBSTANCES OTHER THAN ALDOSTERONE

1962 ◽  
Vol 40 (6) ◽  
pp. 727-738 ◽  
Author(s):  
Wojciech Nowaczynski ◽  
Erich Koiw ◽  
Pierre Biron ◽  
Michel Chrétien ◽  
Jacques Genest
Keyword(s):  
Angiotensin Ii ◽  
Urinary Excretion ◽  
Ultraviolet Light ◽  
Intravenous Infusions ◽  
Human Volunteers

Intravenous infusions of synthetic angiotensin II in human volunteers resulted in the increase of the urinary excretion of at least three ultraviolet light absorbing substances referred to as compounds III, IX, and X. This was concomitant with the increase of the urinary aldosterone excretion.Compound III has been partially described before; this is extended. A brief characterization of compounds IX and X is included (see Appendix).

Urinary Excretion of Aminohydroxypropylidene Bisphosphonate in Cancer Patients after Single Intravenous Infusions

1993 ◽  
Vol 82 (6) ◽  
pp. 665-667 ◽  
Author(s):  
Elliot Redalieu ◽  
Jean M. Coleman ◽  
Keith Chan ◽  
John Seaman ◽  
Peter H. Degen ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Cancer Patients ◽  
Intravenous Infusions

THE URINARY EXCRETION OF TESTOSTERONE AND EPITESTOSTERONE IN FEMALES FOLLOWING INTRAVENOUS INFUSIONS OF TESTOSTERONE BEFORE AND DURING TREATMENT WITH AN ANTI-ANDROGEN (CYPROTERONE)

1968 ◽  
Vol 59 (3) ◽  
pp. 454-458 ◽  
Author(s):  
J. Tamm ◽  
W. Beischer
Keyword(s):  
Urinary Excretion ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Marked Elevation ◽  
Intravenous Infusions

ABSTRACT Intravenous infusions of 10 mg testosterone (T) in two females (one of them adrenalectomized for Cushing's syndrome) resulted in an increased urinary excretion of T-glucuronide, whereas the excretion of epitestosterone (ET)-glucuronide was not altered significantly. The excretion of T-sulphate increased only slightly. During treatment with 100 mg Cyproterone p. d. a marked elevation of urinary T and ET excretion occurred. A slight increase in unconjugated T and ET was also observed. A second T infusion during Cyproterone treatment did not lead to a further increase of urinary T-glucuronide, but there was a slight increase in urinary excretion of ET-glucuronide and of T-sulphate.

The Effect on Appetite in Dogs of Pyrogenic Substances in Intravenous Infusions

1954 ◽  
Vol 27 (3) ◽  
pp. 347-352 ◽  
Author(s):  
W.M. Dale Beamer ◽  
J.E. Thomas ◽  
Beatrice Moore
Keyword(s):  
Intravenous Infusions

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

Cigarette Smoking Increases Thromboxane A2 Formation without Affecting Platelet Survival in Young Healthy Females

1992 ◽  
Vol 68 (05) ◽  
pp. 583-588 ◽  
Author(s):  
Annika Dotevall ◽  
Christina Rångemark ◽  
Elsa Eriksson ◽  
Jack Kutti ◽  
Hans Wadenvik ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cigarette Smoking ◽  
Blood Cell ◽  
Urinary Excretion ◽  
Life Span ◽  
Cell Count ◽  
Thromboxane A2 ◽  
Blood Cell Count ◽  
Platelet Activity ◽  
Pai 1

SummarySmoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volunteers (aged 20–46 years, 18 smokers and 17 non-smokers) platelet life-span and indices of platelet activity were determined, together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen, peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p <0.05), while plasma and urinary β-thromboglobulin, plasma platelet factor 4, platelet mean life-span and platelet production rate did not differ between the groups. PAI-1 activity, white blood cell count and hematocrit were higher in smokers than in non-smokers (p <0.05). These data indicate that smoking facilitates platelet formation of thromboxane A2 without affecting platelet survival; i.e. it increases the activity of platelets without affecting their viability to a measurable extent. Such an increase in platelet activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit and white blood cell count, may play an etiological role in smoking-induced cardiovascular disease in women.

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