Effect of Chronic and Acute Changes in Sodium Balance on the Urinary Excretion of Prostaglandins E2 and F2α in Normal Man

1981 ◽  
Vol 60 (4) ◽  
pp. 405-410 ◽  
Author(s):  
M. Rathaus ◽  
E. Podjarny ◽  
Eli Weiss ◽  
M. Ravid ◽  
Sara Bauminger ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Prostaglandin E2 ◽  
Prostaglandin F2α ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Acute Changes ◽  
Prostaglandins E2 And F2α

1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2α was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing <20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 ± 201.6 sem to 1761.3 ± 304.9 ng/24 h, P<0.0005). Prostaglandin F2α also increased from 1187.0 ± 390.1 to 1435.6 ± 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2α ratio increased from 0.83 ± 0.2 to 1.52 ± 0.34 (P<0.01). Plasma renin activity and aldosterone rose significantly (P<0.05 and<0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 ± 29.9 to 86.7 ± 22.9 ng/h (P<0.05) and to 36.9 ± 5.96 ng/h after 4 h. Prostaglandin F2α decreased at a slower rate, from 98.4 ± 18.7 to 37.5 ± 8.8 ng/h at 4 h (P<0.02). At 4 h the prostaglandin E2/prostaglandin F2α ratio returned to control values (0.90 ± 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P<0.02 and<0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2α and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E2 9-ketoreductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.

Studies on the Renin-Angiotensin System in a Kininogen-Deficient Individual

1983 ◽  
Vol 65 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Patrick Y. Wong ◽  
Gordon H. Williams ◽  
Robert W. Colman
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Normal Individuals

1. The physiological responses of the renin-angiotensin system were studied in an individual with kininogen deficiency (patient 1) with absent plasma bradykinin and markedly impaired prekallikrein conversion into kallikrein. After sodium depletion, patient 1 had a low plasma renin activity (1.4 pmol of ANG I h−1 ml−1) and a low angiotensin II concentration (36 pg/ml) compared with values in 11 normal individuals (4.0 ± 0.94 pmol of ANG I h−1 ml−1) and 63 ±6 pg/ml respectively). 2. Unlike normal individuals, in the kininogen-deficient subject there was no significant fall of renin activity or angiotensin II after dietary sodium repletion. Intravenous sodium repletion also failed to further decrease plasma renin activity or angiotensin II. 3. The usual two- to three-fold rise in plasma renin activity and angiotensin II observed in normal subjects on assumption of the upright posture after ingestion of 200 mg of sodium/day failed to occur in the kininogen-deficient individual. 4. These data in vivo are in agreement with observations in vitro that once plasma kallikrein forms it may be important in converting prorenin into renin. In the absence of kininogen, activation of prekallikrein to kallikrein is grossly defective, which may in part account for the diminished response of the renin-angiotensin system to changes in sodium balance and posture.

VARIATIONS IN PLASMA RENIN ACTIVITY AND URINARY ALDOSTERONE EXCRETION IN NORMAL SUBJECTS AFTER SALT RESTRICTION AND ACUTE PITUITARY INHIBITION WITH 6-DEHYDRO-16-METHYLENE HYDROCORTISONE

1971 ◽  
Vol 67 (1) ◽  
pp. 159-173
Author(s):  
A. Peytremann ◽  
R. Veyrat ◽  
A. F. Muller
Keyword(s):  
Plasma Renin Activity ◽  
Salt Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Sodium Balance ◽  
Experimental Conditions ◽  
Salt Restriction ◽  
Aldosterone Production

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.

Solitary Kidney and Ageing as Causes of Low Renin and Aldosterone Concentrations: Relevance to ‘Low-Renin’ Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Normotensive Subjects ◽  
The Mean

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.

Development of two-kidney Goldblatt hypertension in rats under dietary sodium restriction

1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Goldblatt Hypertension

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

THE EFFECT OF INSULIN INDUCED HYPOGLYCAEMIA ON PLASMA RENIN ACTIVITY AND URINARY CATECHOLAMINES BEFORE AND FOLLOWING CLONIDINE (CATAPRESAN®) IN MAN

1972 ◽  
Vol 71 (2) ◽  
pp. 321-330 ◽  
Author(s):  
H. Hedeland ◽  
J.-F. Dymling ◽  
B. Hökfelt
Keyword(s):  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Adrenal Medulla ◽  
Sympathetic Nerve ◽  
Plasma Renin ◽  
Renin Activity ◽  
Nerve Endings ◽  
Urinary Catecholamines ◽  
A Minor ◽  
Noradrenaline And Adrenaline

ABSTRACT The present study was concerned with the relation of catecholamine production and plasma renin activity. The catecholamine production was measured as the urinary excretion of noradrenaline and adrenaline. Thirteen subjects were studied under basal conditions and also following insulin induced hypoglycaemia both before and during treatment with the imidazoline derivate clonidine. Before clonidine, hypoglycaemia produced a marked increase in catecholamine production and an elevation of plasma renin activity. These parameters were significantly correlated. Treatment with clonidine markedly suppressed noradrenaline production and plasma renin activity. Adrenaline production showed a minor decrease. During clonidine treatment insulin induced pronounced hypoglycaemia. In spite of this the increase in adrenaline production and plasma renin activity was less marked as compared to that before clonidine. There was no longer any significant correlation between catecholamine production and plasma renin activity. Our results indicate that sympathetic amines liberated from the adrenal medulla and/or the sympathetic nerve endings can stimulate renin production.

scholarly journals Plasma Renin Activity Related to Sodium Balance, Renal Function and Urinary Vasopressin in the Newborn Infant

1979 ◽  
Vol 13 (6) ◽  
pp. 742-745 ◽  
Author(s):  
Claude Godard ◽  
Jean-Marc Geering ◽  
Katy Geering ◽  
Michel B Vallotton
Keyword(s):  
Renal Function ◽  
Plasma Renin Activity ◽  
Newborn Infant ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance

The Effect of Mental Stress on Catecholamines, their Metabolites and Plasma Renin Activity in Patients with Essential Hypertension and in Healthy Subjects

1979 ◽  
Vol 57 (s5) ◽  
pp. 229s-231s ◽  
Author(s):  
W. Januszewicz ◽  
M. Sznajderman ◽  
B. Wocial ◽  
T. Feltynowski ◽  
T. Klonowicz
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Mental Stress ◽  
Healthy Subjects ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vanillylmandelic Acid ◽  
Before And After ◽  
Noradrenaline And Adrenaline

1. Ten patients with essential hypertension and ten healthy men were submitted to mental stress consisting of Kraepelin's arithmetic test combined with noise. Concentrations of plasma and urine catecholamines and of their metabolites as well as plasma renin activity before and after the test were studied. 2. In both groups a significant increase of noradrenaline and adrenaline in blood and noradrenaline in urine was observed. The urinary excretion of dopamine fell significantly in both groups after stress. 3. After mental stress a significant increase in urinary excretion of 3-methoxy-4-hydroxyphenylglycol was observed in both groups. The excretion of vanillylmandelic acid decreased significantly only in healthy subjects. 4. The plasma renin activity rose significantly in both groups but the increase was more pronounced in healthy subjects.

Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Concurrent Administration ◽  
Angiotensin System

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

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