Sodium Balance, Urinary Prostaglandin E2 and Renin in Normal Man

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.

1971 ◽  
Vol 67 (1) ◽  
pp. 159-173
Author(s):  
A. Peytremann ◽  
R. Veyrat ◽  
A. F. Muller

ABSTRACT Variations in plasma renin activity and urinary aldosterone excretion were studied in normal subjects submitted to salt restriction and simultaneous inhibition of ACTH production with a new synthetic steroid, 6-dehydro-16-methylene hydrocortisone (STC 407). At a dose of 10 mg t. i. d. this preparation exerts an inhibitory effect on the pituitary comparable to that of 2 mg of dexamethasone. In subjects maintained on a restricted salt intake, STC 407 does not delay the establishment of an equilibrium in sodium balance. The increases in endogenous aldosterone production and in plasma renin activity are also similar to those seen in the control subjects. A possible mineralocorticoid effect of STC 407 can be excluded. Under identical experimental conditions, the administration of dexamethasone yielded results comparable to those obtained with STC 407.


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

1986 ◽  
Vol 70 (5) ◽  
pp. 523-526 ◽  
Author(s):  
P. Coruzzi ◽  
A. Biggi ◽  
L. Musiari ◽  
C. Ravanetti ◽  
P. P. Vescovi ◽  
...  

1. Natriuresis was studied during water immersion in eight normal subjects either in the absence or in the presence of dopamine blockade by domperidone. 2. Creatinine clearance showed no significant changes; urine flow remained significantly above control values during water immersion, implying persistent suppression of antidiuretic hormone. 3. The marked natriuresis seen during water immersion alone was significantly blunted (P < 0.05) but not abolished during water immersion plus domperidone. 4. Suppression of the renin–aldosterone system by water immersion alone was not significantly different from that obtained during water immersion plus dopamine blockade. 5. On the contrary, plasma prolactin levels, previously suppressed during water immersion alone, were significantly stimulated during water immersion plus domperidone, thus indirectly suggesting a role of dopamine in mediating the blunted natriuresis seen during water immersion.


2001 ◽  
Vol 281 (6) ◽  
pp. R1887-R1894 ◽  
Author(s):  
Christopher J. Charles ◽  
M. Gary Nicholls ◽  
Miriam T. Rademaker ◽  
A. Mark Richards

The role of adrenomedullin (ADM) in volume and pressure homeostasis remains undefined. Accordingly, we compared the biological responses to infusions of ADM and nitroprusside (NP; matched for reduction of arterial pressure) and assessed their effects on responses to ANG II and norepinephrine in eight conscious sheep. During matched falls in arterial pressure (8–10 mmHg, both P < 0.001) ADM and NP induced similar increases in heart rate. ADM increased cardiac output ( P < 0.001), and the fall in calculated peripheral resistance was greater with ADM than NP ( P = 0.013). ADM infusions raised plasma ADM levels ( P < 0.001), plasma renin activity ( P = 0.001), and ANG II ( P < 0.001) but tended to blunt any concurrent rise in aldosterone compared with NP ( P = 0.056). ADM maintained both urine flow ( P < 0.001) and sodium excretion ( P = 0.01) compared with falls observed with NP. ADM attenuated the vasopressor actions of exogenous ANG II ( P = 0.006) but not norepinephrine. In addition, ADM antagonized the ANG II-induced rise in plasma aldosterone ( P < 0.001). In conclusion, ADM induces a different spectrum of hemodynamic, renal, and endocrine actions to NP. These results clarify mechanisms by which ADM might contribute to volume and pressure homeostasis.


1976 ◽  
Vol 230 (2) ◽  
pp. 311-318 ◽  
Author(s):  
TE Lohmeier ◽  
JO Davis

Hypertension was produced in 25 rabbits by constricting the right renal artery and leaving the opposite kidney intact (two-kidney hypertension). After 30 days mean arterial pressure and plasma renin activity (PRA) were significantly elevated (P less than 0.01), and arterial pressure was correlated with PRA (r = 0.551, P less than 0.01); however, not all hypertensive rabbits had elevated PRA, and in animals in which sodium balance was monitored, only rabbits in negative sodium balance had increased levels of PRA. To investigate the role of angiotensin II (A-II) in the hypertension, [1-sarcosine,8-alanine]angiotensin II was infused at 6 mug/kg per min for 30 min in anesthetized hypertensive animals (n = 25). For the group, arterial pressure fell significantly (P less than 0.01), but several animals with minimal hypertension failed to give a depressor response. The declines in arterial pressure were highly correlated with PRA (r = 0.853, P less than 0.01). Aldosterone secretion in hypertensive animals was correlated with PRA (r = 0.851, P less than 0.01). Thus, two-kidney hypertension in the rabbit persists with normal PRA, but during periods of spontaneous sodium depletion, A-II plays a role in the maintenance of the hypertension.


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.


1977 ◽  
Vol 53 (4) ◽  
pp. 321-328 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
J. D. H. Slater

1. The renal excretion of sodium by five patients with autonomic failure (Shy—Drager syndrome) was compared with a matched control group who had normal autonomic reflexes (Parkinson's disease). For 8 or 9 days the daily sodium intake was reduced to 17 mmol, and for 5 subsequent days it was increased to 189 mmol. 2. The sodium excretion of the patients with autonomic failure was not significantly reduced during 7 days of restricted intake whereas that of the control group fell rapidly to values comparable with their sodium intake. Patients with autonomic failure had a larger fall in body body weight than the control subjects. 3. Both lying and standing values of mean blood pressure fell during salt restriction in the patients with autonomic failure, but not in the control subjects. 4. Values of plasma renin activity (PRA) were significantly depressed in patients with autonomic failure. However, PRA rose to values similar to those of control subjects while standing during the period of restricted sodium intake. At this time the patients with autonomic failure had a large orthostatic fall in blood pressure and creatinine clearance. 5. Aldosterone secretion rates were measured in three patients with autonomic failure at both levels of sodium intake and were considerably lower than the rates found in the control group. 6. A mineralocorticoid drug (9α-fludrocortisone; 2 mg/day), given on the last 2 days of restricted sodium intake, failed to correct fully the negative sodium balance of the patients with autonomic failure, since an excessive sodium excretion persisted during the period of recumbency at night. 7. These results demonstrate a severe defect in renal salt conservation in certain patients with autonomic failure. They suggest that the defect may not be entirely due to deficient secretion of mineralocorticoid hormones.


2012 ◽  
Vol 50 (01) ◽  
Author(s):  
N Lange ◽  
S Sieber ◽  
A Erhardt ◽  
G Sass ◽  
HJ Kreienkamp ◽  
...  

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