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The effects of infusions of equimolar doses of Sar1-Ile8-angiotensin II and of Sar1-Ala8-angiotensin II on plasma aldosterone, plasma renin activity and arterial blood pressure were compared in normal dogs. Plasma aldosterone increased significantly after Sar1-Ile8-angiotensin II whereas it was unaffected by Sar1-Ala8-angiotensin II. Changes in blood pressure and renin activity were small without marked differences between both groups of animals. The experiments demonstrate a clear steroidogenic potency of Sar1-Ile8-angiotensin II. Therefore, Sar1-Ala8-angiotensin II should be preferred as antagonist of the action of angiotensin II in the adrenal gland.

In two patients with terminal renal failure the night-day rhythm of plasma aldosterone (PA) renin activity (PRA) and plasma cortisol (PC) were examined before and after bilateral nephrectomy and after renal transplantation. Before nephrectomy changes in abnormally high PA coincided with PC whereas no significant correlation was observed between PA and PRA. In the anephric state secretory episodes of PA occurred independent from those of PC while PRA was undetectable. After renal transplantation a lack of night-day variation in renin secretion was observed in both patients; only one of the two patients showed episodic secretion of PA while PC was suppressed in both patients probably due to the chronic administration of prednisone. Our results indicate, that before nephrectomy under the conditions described in this study plasma aldosterone was predominantly controlled by ACTH. In the anephric state and after renal transplantation other (yet unidentified) factors might have caused episodic secretion of aldosterone. Finally, the lack of night-day variation and secretory episodes in renin secretion after transplantation points to an important role of the sympathetic nervous system in the control of circadian and episodic renal renin release.

Supine plasma aldosterone and plasma renin activity were determined in patients with cirrhosis of the liver and ascites (n = 10). Most of the patients initially showed an increase in plasma aldosterone and plasma renin activity. However, values within the normal range were observed (plasma aldosterone, n = 3; plasma renin activity, n = 4). In the ascitic fluid renin activity could not be detected, whereas aldosterone concentrations correlated significantly with the respective plasma levels (r = 0.8, p less than 0.01). During therapy with spironolactone alone (n =2) or in combination with furosemide (n = 4), diuresis and natriuresis showed no correlation with changes in plasma aldosterone and/or plasma renin activity. Our results suggest that other factors than renin and aldosterone secretion may be important in the formation of ascites in patients with cirrhosis of the liver. In addition, the inverse correlation between mean arterial blood pressure and plasma renin activity (r = -0.65, p less than 0.05) found in our patients supports the assumption that the increase in renin secretion is probably induced by changes in (renal) hemodynamics.

Plasma aldosterone, plasma cortisol and the serum concentrations of sodium and potassium were determined in 5 anephric patients before and at short time intervals up to 180 minutes after hemodialysis. Plasma aldosterone increased in 4 of 5 patients during hemodialysis while in all patients plasma cortisol, sodium and potassium decreased. Only one patient showed a fall in aldosterone during hemodialysis. After hemodialysis plasma aldosterone gradually decreased over a period of 3 hours in 3 of 5 patients, whereas the remaining two patients showed typical secretory episodes of aldosterone. In each patient serum potassium rapidly increased while serum sodium showed only minor variations. Plasma cortisol followed the normal circadian rhythm. We suggest that a still unkown factor had caused the observed increases in plasma aldosterone during hemodialysis. There are reasons to believe that over the period observed after hemodialysis the intracellular potassium concentration and not serum potassium levels has influenced adrenal aldosterone release. This would explain the paradoxical decrease in plasma aldosterone in 3 of the 5 patients while serum potassium increased.

In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 mug/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not be related to its vasoconstrictive activity.

In order to elucidate the main factors controlling plasma aldosterone in infancy and childhood, plasma renin activity (PRA), plasma cortisol (PC, as a parameter of ACTH activity), plasma aldosterone (PA) and serum sodium and potassium were measured simultaneously in 84 healthy children (62 recumbent, 22 upright) ranging in age from 6 days to 16 years. 10 healthy male students served as adult controls. As compared to the controls, PRA levels were significantly higher in the children up to the age of 12 years. PA was also elevated in most children; the highest values for PA and for PRA were observed during the first 4 years of life. A significant positive correlation between PRA and PA (n = 84, r = 0,62, p less than 0.001) was found. There were no significant differences in serum sodium or potassium or in PC. All PC values were - with one exception - within the range found in healthy adults. Our results indicate that high PA values are freuqently observed in healthy children. They are mainly caused by elevated PRA. The physiological significance of increased activation of the renin-angiotensin-aldosterone system in infancy is not yet clear.

Plasma aldosterone, plasma renin activity (PRA), plasma cortisol as parameter of ACTH activity and the serum concentrations of sodium and potassium were determined at short time intervals in 10 healthy students after an overnight bedrest and during three hours of ambulation. While PRA rose significantly within 15 minutes of orthostasis in all students, plasma aldosterone showed a similar rapid increase in some of the subjects only. These persons demonstrated also a simultaneous increase of serum potassium or of plasma cortisol. Plasma aldosterone rose not before 30 to 60 minutes after change to the upright position in subjects who showed neigher plasma cortisol nor serum potassium increases. It is concluded that the immediate rise of plasma aldosterone during orthostasis seems to depend on a stimulation by ACTH of by potassium. The main stimulus of plasma aldosterone during orthostasis appears to be the renin angiotensin system. If the aldosterone response to posture is mediated only through this system a delay of 30 to 60 minutes is observed.

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of Des -angiotensin II (heptapeptide) on plasma renin activity, blood pressure and plasma aldosterone were compared in normal anaesthetized dexamethasone-suppressed dogs. 2. Plasma renin activity was equally suppressed by both compounds. The increase in blood pressure induced by the heptapeptide averaged 43-62% of the increase during AII infusions. No significant differences in aldosterone increase were observed between AII and the heptapeptide. Plasma aldosterone, however, dropped significantly faster in heptapeptide-treated dogs after the end of the infusions. 3. Sar -Ala -angiotensin II (saralasin, 400 pmol min-1 kg-1) suppressed plasma aldosterone that was stimulated by heptapeptide (20 pmol min-1 kg-1) completely. The same angiotensin antagonist had only a moderate effect on plasma aldosterone stimulated by AII. After stopping the antagonist infusion, plasma aldosterone rose significantly higher in dogs infused with AII than in those receiving the heptapeptide. 4. The results demonstrate differences between the effects of AII and the heptapeptide both on blood pressure and on plasma aldosterone. They do not support the hypothesis that the heptapeptide may be the main mediator of aldosterone secretion.

1. Rabbits were actively immunized aganist angiotensin II (AII). 2. Basal plasma aldosterone concentration was 0-058 plus or minus 0-027 pmol/ml (20-7 plus or minus 9-6 pg/ml) (mean plus or minus SD) in immunized and 0-056 plus or minus 0-021 pmol/ml (20-2 plus or minus 7-5 pe. When the endogenous formation of AII was stimulated by frusemide, by haemorrhage or by feeding with low sodium diet, a significant increase of plasma aldosterone was observed with no difference between immunized and non-immunized animals. 3. In non-immune rabbits, the average mean arterial blood pressure rose 13 mmgHg during the infusion of AII (5 pmol min--1 kg-1) and 27 mmHg during the infusion of 50 pmol min-1 kg-1. In contrast, there was no clear increase in blood pressure in the immunized animals. The blood pressure rose in immune animals (15 mmHg) and in non-immune animals (36 mmHg) during the infusion of 200 pmol min-1 kg-1 ALL. Plasma aldosterone rose in all animals in response to each of the three infusions with no significant difference between the two groups. 4. It is concluded that the immunization against ALL blocked only the pressor effect of the peptide but had no clear influence on the response of plasma aldosterone to increased ALL. Differences between the affinities of the adrenal and vascular AII receptors may explain these findings.

Three antisera specific to aldosterone and elicited with different aldosterone protein conjugates (aldosterone-3-oxine rabbit serum albumin and aldosterone-3-oxime bovine gamma-globulin) were studied by radioimmunological methods at various times subsequent to first-immunization. A considerable variability of the parameters important in radioimmunoassay was observed over the whole experimental period. Titer, sensitivity and specificity of two antisera tended to increase as long as the animals were boosted. In the third they did not change in a uniform way.

The control of plasma aldosterone during hemodialysis was investigated in 31 patients with terminal renal failure. While before hemodialysis renin predominantly influenced aldosterone, this effect dissipated during hemodialysis. In addition, no relationship was observed between changes in aldosterone and those in sodium, potassium and plasma cortisol. In a group of 10 patients isokalemic and isonatremic hemodialysis failed to document an effect sodium or potassium on hemodialysis induced changes in aldosterone. Our data suggest that none of the four factors - renin, ACTH, sodium and potassium - had constantly caused the observed changes in aldosterone during hemodialysis.

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