Search

1. Since important interrelationships between haemodynamic and hormone indices are possible in cardiac failure, measurements of cardiac output, mean pulmonary artery pressure, plasma renin activity, angiotensin II and aldosterone were carried out before and during acute and chronic frusemide therapy in patients with oedematous heart failure who had been given digoxin. 2. Cardiac output fell significantly 90 min after acute frusemide injection, then returned to baseline. Mean pulmonary artery pressure declined steadily throughout the 4 h of observation. 3. These haemodynamic changes occurred in the absence of major hormonal fluctuations and related presumably to direct vascular and diuretic actions of frusemide. 4. With more chronic (8–10 days) oral frusemide therapy, reciprocal changes between haemodynamic and hormone indices were observed. As the diuretic response to frusemide diminished, cardiac output and pulmonary artery pressure declined whereas the renin-angiotensin system was activated. Statistically significant inverse correlations were observed between these haemodynamic and hormone indices. 5. In both acute and chronic phases of the study, fluctuations in aldosterone levels were regulated by the renin-angiotensin system whereas ACTH, plasma potassium and plasma sodium played, at best, supportive roles.

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone responses were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose—response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose—response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4–6 mmol/l. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.

1. To assess whether the adrenal corticosteroid 18-hydroxy-11-deoxycorticosterone [18-(OH)DOC] affects urine electrolyte excretion in normal man, seven male volunteers received 120 µg (353 nmol) intravenously in 1 h. This was compared with glucose (50 g/l; control) and aldosterone (80 µg, 222 nmol) infusions in the same subjects. 2. A definite though weak antinatriuretic response to 18-(OH)DOC was observed, whereas urine potassium excretion was not altered. Aldosterone increased urine potassium excretion and reduced sodium output. Urine pH was lowered by both corticosteroids, aldosterone in general having a more marked effect. Urine volume was not altered by 18-(OH)DOC. 3. Plasma concentrations of 18-(OH)DOC and aldosterone rose approximately tenfold during their respective infusions. Compared with that of aldosterone, the metabolic clearance rate of 18-(OH)DOC was slower and its plasma half-life was longer. 4. We have been able to demonstrate that 18-(OH)DOC has a definite, albeit weak antinatriuretic action in normal man, but whether or not this corticosteroid is capable of elevating the blood pressure in man remains to be shown.

1. Plasma aldosterone concentration and urine aldosterone excretion were studied before and during sustained diuresis in six patients with gross congestive heart failure, under conditions of fixed sodium and potassium intake and strict control of body posture. Simultaneous measurements of plasma renin activity, plasma corticotrophin and electrolytes were made to assess the relative importance of these factors in the regulation of aldosterone secretion before and during treatment of congestive heart failure. 2. During the pre-treatment phase aldosterone levels were normal or raised, but with acute diuresis fell to unmeasurable levels in most cases. This depression in aldosterone tended to coincide with peak natriuresis. Later in the diuretic phase aldosterone values increased often to very high levels as dry body weight was attained. 3. With few exceptions plasma renin activity fluctuations paralleled those of plasma aldosterone, whereas corticotrophin levels remained largely within normal limits and plasma electrolytes did not change appreciably. 4. The results suggest that the renin—angiotensin system is the important regulator of aldosterone secretion before and during diuretic treatment in patients with gross congestive heart failure.

1. Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3–3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). 2. Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. 3. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. 4. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. 5. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. 6. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.