The relationship of urinary prostaglandins and plasma renin to sodium balance and diuresis in normal man

1979 ◽  
Vol 3 (4) ◽  
pp. 235-247 ◽  
Author(s):  
B. Hesse ◽  
P. Christensen ◽  
J. Elmgreen ◽  
I. Nielsen
1970 ◽  
Vol 39 (3) ◽  
pp. 437-455 ◽  
Author(s):  
R. H. Chinn ◽  
J. J. Brown ◽  
R. Fraser ◽  
Sheila M. Heron ◽  
A. F. Lever ◽  
...  

1. The relationship of changes in plasma renin and plasma aldosterone concentration to electrolyte balance was studied during total fasting and during sodium deprivation followed by total fasting. 2. During simple sodium deprivation obese subjects lost significantly more sodium than lean subjects, but the rise in plasma renin concentration (PRC) was similar in the two groups. 3. During total fasting there was a failure of PRC to increase in the expected manner despite a marked negative sodium balance. In the early stages of the fast, PRC decreased in nine of eleven subjects while subsequently it increased in all subjects. 4. During sodium deprivation PRC and plasma aldosterone concentration (PAC) rose in all subjects studied, but in the first few days of a period of total fasting immediately following, there was a fall in PRC in eight of ten subjects studied, while PAC continued to rise in five of six subjects in whom it was measured. 5. These results are discussed in relation to the concept of the renin-angiotensin system as a regulator of aldosterone secretion.


1986 ◽  
Vol 250 (2) ◽  
pp. R287-R291
Author(s):  
C. E. Wade ◽  
L. C. Keil ◽  
D. J. Ramsay

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.


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.


1978 ◽  
Vol 55 (s4) ◽  
pp. 377s-379s ◽  
Author(s):  
C. E. Grim ◽  
M. H. Weinberger ◽  
D. P. Henry ◽  
F. C. Luft ◽  
N. S. Fineberg

1. Blood pressure, plasma renin activity, plasma aldosterone, urinary noradrenaline during sleep (UNA-S) and several estimates of sodium intake were determined in 379 normotensive subjects (age 13–70) to investigate the relationship of these variables to blood pressure. 2. Blood pressure was correlated with age, weight, plasma renin activity UNA-S, and estimates of sodium intake. These variables were frequently intercorrelated. 3. Multiple-correlation analysis revealed that after removal of the effects of age, blood pressure was related to weight, plasma renin activity, UNA-S and estimates of sodium intake. 4. However, multiple-regression analysis failed to demonstrate an effect of plasma renin activity, UNA-S, or estimates of sodium intake on blood pressure when the effects of age, weight, race and sex were removed. 5. Careful matching of subjects by age, weight, race and sex in studies of blood pressure and biochemical factors in normal subjects is crucial to proper interpretation of such data.


1988 ◽  
Vol 255 (2) ◽  
pp. R274-R283 ◽  
Author(s):  
D. C. Curran-Everett ◽  
J. R. Claybaugh ◽  
K. Miki ◽  
S. K. Hong ◽  
J. A. Krasney

Hypoxia alters the relationship of aldosterone secretion to plasma renin activity. The potential role plasma electrolytes play in this modification is not clear. This study analyzed the interrelationships among renin, aldosterone, vasopressin (ADH), and plasma electrolytes during 96 h of normobaric hypoxia. Eight ewes were exposed, in discrete experiments, to hypocapnic hypoxia [arterial O2 tension (PaO2) 37-42 mmHg, arterial CO2 tension (PaCO2) 26-28 mmHg] and eucapnic hypoxia (PaO2 40-43 mmHg, PaCO2 28-31 mmHg) by N2 dilution in an environmental chamber. Urine output (24 h) was measured, and arterial plasma samples were collected during the normoxic control period and at 24-h intervals of hypoxia. Plasma Na+, K+, renin, and ADH levels did not change from the normoxic values during either hypocapnic or eucapnic hypoxia. However, urinary aldosterone excretion [critical significance (alpha) less than 0.046] and K+ excretion (alpha less than 0.046) decreased markedly during each type of hypoxia. All sheep developed a pronounced negative K+ balance by 96 h of hypoxia. These data suggest that plasma K+ concentration is preserved by movement of K+ out of the intracellular compartment; this change in K+ distribution may inhibit aldosterone secretion during hypoxia.


1996 ◽  
Vol 270 (4) ◽  
pp. H1200-H1206 ◽  
Author(s):  
P. A. Modesti ◽  
I. Cecioni ◽  
A. Naldoni ◽  
A. Migliorini ◽  
G. G. Neri Serneri

The present study was performed in seven healthy subjects (aged 22-35 years) to investigate 1) whether plasma and urinary endothelin-1 (ET-1) are involved in the response to postural changes and 2) the relationship between ET-1 formation and the renin-angiotensin system (RAS). Six hours of standing caused a prompt but very short-lasting increase in plasma ET-1 concentration (59% after 5 min, 12% after 1 h) and a notable and sustained enhancement of urinary ET-1 excretion (from 0.59 +/- 0.10 to 1.43 +/- 0.28 pg/min, or 142%; P < 0.001). Plasma renin activity increased by 169% after 1 h of standing. A parallel contraction of urinary volume (-62%), sodium excretion (-55%), and free water reabsorption (-24%) occurred. The return to the supine position after 6 h of orthostasis caused a reduction to baseline values of the ET-1 urinary excretion and urinary volume within 2 h. Inhibition of angiotensin-converting enzyme blunted, but did not eliminate, the orthostasis-induced increase in ET-1 urinary excretion (100%, P < 0.002) and changes in the renal functions. The present results indicate that renal ET-1 is involved in the hemodynamic long-lasting responses to postural changes and that its increase is partially controlled by RAS and suggest that ET-1 might play a role in the regulation of renal function in humans.


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