Renal prostaglandins and sodium balance in normal man

1979 ◽  
Vol 2 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Z. Kaye ◽  
R.D. Zipser ◽  
S. Mayeda ◽  
P.K. Zia ◽  
R. Horton
1979 ◽  
Vol 57 (s5) ◽  
pp. 267s-269s ◽  
Author(s):  
I. Nielsen ◽  
J. Elmgreen ◽  
P. Christensen ◽  
B. Hesse

1. Urinary prostaglandin (PG) E2 excretion and plasma renin were measured in five healthy volunteer subjects for 2 h after intravenous injection of frusemide (protocol A) and during salt restriction for 7 days with frusemide added on the 2 last days (protocol B). 2. In protocol A, peak values in PGE2 and urine flow were reached in 10–20 min, after which the values rapidly subsided. Plasma renin increased twofold in 60 min. 3. In protocol B, even during severe anti-natriuresis (day 5) and during maximal negative sodium balance (day 7), no change in urinary PGE2 excretion was observed. Plasma renin increased twofold on day 5 and increased tenfold on day 7. 4. The result of protocol B does not suggest any essential role of renal PGE2 for sodium excretion or sodium homeostasis in man. The result of protocol A may point to a role of renal prostaglandins for the diuretic action of frusemide.


1979 ◽  
Vol 3 (4) ◽  
pp. 235-247 ◽  
Author(s):  
B. Hesse ◽  
P. Christensen ◽  
J. Elmgreen ◽  
I. Nielsen

1964 ◽  
Vol 207 (1) ◽  
pp. 104-108 ◽  
Author(s):  
Donald S. Gann ◽  
Catherine S. Delea ◽  
John R. Gill ◽  
J. Picton Thomas ◽  
Frederic C. Bartter

Seven normal subjects were subjected to depletion and repletion of body potassium on balance regimen. Aldosterone excretion, plasma volume, and arterial pressure were measured. Potassium depletion decreased and potassium repletion consistently increased aldosterone excretion. Changes in sodium balance were prevented by restricting dietary sodium or replacing lost sodium. The effects on aldosterone excretion were thus shown to be independent of reciprocal changes in sodium balance of intravascular volume or of arterial pressure. The results suggest that changes in body potassium influence aldosterone secretion by mechanisms independent of those responsive to changes in body sodium or fluid volume.


1983 ◽  
pp. 167-175 ◽  
Author(s):  
M. B. Vallotton ◽  
L. Favre ◽  
P. Glasson ◽  
J. Dürr ◽  
M. Bonhomme ◽  
...  

1970 ◽  
Vol 28 (3) ◽  
pp. 312-317 ◽  
Author(s):  
N. K. Hollenberg ◽  
M. Epstein ◽  
R. D. Guttmann ◽  
M. Conroy ◽  
R. I. Basch ◽  
...  

2009 ◽  
Vol 46 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Tatjana Davila ◽  
Dusan Davila ◽  
Ernst Oliw ◽  
Erik Änggård

1997 ◽  
Vol 23 (4) ◽  
pp. 377-392 ◽  
Author(s):  
Michael S. Gordon ◽  
Joseph A. Majzoub ◽  
Gordon H. Williams ◽  
Murray B. Gordon
Keyword(s):  

1970 ◽  
Vol 39 (5) ◽  
pp. 641-651 ◽  
Author(s):  
F. J. Goodwin ◽  
J. G. G. Ledingham ◽  
J. H. Laragh

1. Vasopressin was administered to normal men in metabolic balance for periods of 5–10 days under conditions of water restriction or overhydration. Likewise, oxytocin was administered to two normal men for 10 days. 2. The effects of both neuropeptides on plasma renin activity, aldosterone excretion rate and sodium balance were observed. 3. In the absence of overhydration, vasopressin had no demonstrable effect upon plasma renin activity, aldosterone excretion rate or sodium balance. During overhydration body weight gain and plasma dilution were followed by natriuresis; the associated changes in plasma renin activity and aldosterone excretion, however, were unimpressive. 4. The prolonged administration of oxytocin for 10 days under conditions of normal hydration failed to influence sodium excretion, plasma renin activity or aldosterone excretion. 5. It is concluded that in normal man changes in circulating levels of vasopressin or oxytocin do not play a physiological role in the control of sodium excretion.


2012 ◽  
Vol 37 (03) ◽  
Author(s):  
N Rakova ◽  
K Jüttner ◽  
M Rauh ◽  
A Dahlmann ◽  
U Goller ◽  
...  
Keyword(s):  

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.


Sign in / Sign up

Export Citation Format

Share Document