Basal Plasma Aldosterone Concentration Research Articles

Renin-angiotensin system and plasma aldosterone in Cushing's syndrome.

The renin-angiotensin system was studied in eight patients with Cushing's syndrome (four with adrenal adenoma and four with adrenal hyperplasia) and in five normal controls. Basal plasma renin activity (PRA) and aldosterone concentration (PAC) were similar in supine position among Cushing's syndrome due to adrenal adenoma (PRA; 1.0 +/- 0.3 ng/ml/h, PAC; 7.4 +/- 1.0 ng/dl, mean +/- SE), those due to adrenal hyperplasia (1.0 +/- 0.2, 6.9 +/- 0.8) and the controls (0.8 +/- 0.1, 6.4 +/- 0.4). The PRA after furosemide (1 mg/kg i.v.) and 120 min. upright posture stimulation was similar among Cushing's syndrome due to adrenal adenoma (2.2 +/- 0.7 ng/ml/h), those due to adrenal hyperplasia (2.6 +/- 1.7) and the controls (2.5 +/- 1.2). However, the PAC response after the stimulation in Cushing's syndrome due to adrenal hyperplasia (7.1 +/- 1.2 ng/dl) was significantly lower than that in the controls (17.5 +/- 2.1) (p less than 0.01), although there was no significant difference between the PAC response in Cushing's syndrome due to adrenal adenoma (12.6 +/- 1.0) and the controls. These results indicate that PAC response to furosemide and upright pasture stimulation might be suppressed in Cushing's syndrome due to adrenal hyperplasia.

Acute dopaminergic inhibition of aldosterone secretion is independent of angiotensin II and adrenocorticotropin.

To clarify whether dopaminergic inhibition of aldosterone secretion is physiologically dependent on stimuli from tropic hormones, we attempted to block angiotensin II (AII)- and ACTH-mediated increases in the plasma aldosterone concentration (PAC) with dopamine in normal human subjects. The effect of dopamine on metoclopramide-induced aldosterone secretion also was studied. Six normal male subjects in metabolic balance on a 150 meq/day sodium and 60 meq/day potassium intake received AII infusion at 2, 4, and 6 pmol/kg . min, each dose for 30 min, on each of 2 consecutive days. On the first day, the subjects received a vehicle infusion from 60 min before to the end of the AII infusion; on the second day, dopamine (4 micrograms/kg . min) was substituted for vehicle. AII in the presence of vehicle increased PAC from 5.4 +/- 1.3 to 19.9 +/- 2.9 ng/100 ml; AII in the presence of dopamine increased PAC from 4.8 +/- 0.5 to 19.5 +/- 1.8 ng/100 ml (P = NS). After an interval of 3 weeks on an ad libitum diet, the same protocol was repeated except that ACTH (5, 10, and 20 U/h) was substituted for AII. ACTH in the presence of vehicle increased PAC from 8.1 +/- 2.7 to 27.3 +/- 3.1 ng/100 ml; in the presence of dopamine, ACTH increased PAC from 4.7 +/- 0.5 to 34.9 +/- 6.1 ng/100 ml (P = NS). Metoclopramide increased PAC from 4.5 +/- 0.6 to 17.8 +/- 2.3 ng/100 ml in the presence of vehicle and from 4.4 +/- 0.5 to 7.2 +/- 0.7 ng/100 ml in the presence of dopamine (P less than 0.01). Dopamine did not decrease basal PAC. Dopamine inhibits increases in aldosterone secretion induced by dopamine antagonist but does not alter AII- or ACTH-induced steroid secretion. Acutely, dopaminergic inhibition of aldosterone secretion is independent of AII and ACTH.

Ontogeny of blood pressure and the renin-angiotensin-aldosterone system. Sequential studies in the newborn lamb.

To test the hypothesis that the rise in arterial pressure occurring with maturation is due to an increase in the vascular responsiveness to angiotensin II, sequential cumulative doses of angiotensin II were infused intravenously into chronically catheterized newborn lambs maintained on a constant, weight-adjusted sodium intake from birth to 8 weeks of age. Basal mean arterial pressure correlated with both age and weight, but age was a stronger determinant of mean arterial pressure than was weight. No change in the mean arterial pressure response to angiotensin II occurred with maturation. Basal plasma renin activity and plasma aldosterone concentrations were low and did not change significantly with age. Therefore, in the newborn lamb in the sodium replete state, age is a better determinant of arterial pressure than is weight. However, an age-related change in vasoconstrictor responsiveness to angiotensin II does not occur and, therefore, cannot account for the rise in arterial pressure that is observed with maturation.

Aldosterone Response to ACTH Stimulation in Anephric and Non‐nephrectomized Patients on Regular Hemodialysis

The effect of ACTH on plasma aldosterone concentration (PAC) and plasma cortisol concentration (PCC) has been investigated in 5 anephric and 6 non-nephrectomized patients on regular homodialysis. Basal PAC was significantly lower (p less than 0.01) in the anephric (mean 37.6 pg/ml) than in the nonnephrectomized group (mean 117.5 pg/ml), whereas basal PCC (18.6 and 16.5 mug/100 ml, respectively) did not differ significantly (p less than 0.05). Following administration of synthetic beta1-24 ACTH, the maximal percentage increase in PAC was significantly lower ( less than 0.001) in the anephric (105%) than in the nonnephrectomized group (286%). The rise in PCC, 118%, in both groups showed no significant difference (p less than 0.05). The higher basal level of PAC and the more pronounced response to ACTH in nonnephrectomized patients correlated with higher basal levels of plasma renin activity compared with the anephric group. An influence of the remaining renin-angiotensin system on the ability to react to an ACTH stimulation is therefore suggested.

Outpatient Screening Tests for Primary Aldosteronism

The assessment of basal plasma aldosterone and renin concentrations, and urinary aldosterone excretion has been compared with their values after a suppressive test employing mineralocorticoid induced volume expansion in five patients with primary aldosteronism and in patients with essential hypertension. Reliance upon measurements of basal plasma aldosterone concentration, plasma renin/aldosterone ratio and urine aldosterone excretion alone proved unsatisfactory for distinguishing patients with primary aldosteronism. However these patients, in contrast to those with essential hypertension, showed elevated values or no decrease in plasma aldosterone concentration following three days treatment with 400 mug fludrocortisone (florinef) daily. It is proposed that the assessment of basal plasma renin activity together with florinef suppression of plasma aldosterone are the most effective and convenient outpatient screening procedures in the diagnosis of primary aldosteronism.

Effect of immunization against angiotensin II on blood pressure and on plasma aldosterone in the rabbit.

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.

Control of aldosterone responsiveness in terminal renal failure

Control of aldosterone responsiveness in terminal renal failure. Plasma aldosterone concentration in 30 hemodialysis patients correlated closely with renin concentration, renin activity or renin and potassium concentrations combined (r is greater than or equal to 0.62; P is less than 0.01), and increased consistently in response to upright posture or corticotropin administration. Aldosterone response to hemodialysis was variable. Significant correlations (r is greater than or equal to 0.65; P is less than 0.01) were demonstrated between postural plasma aldosterone and renin responses, between aldosterone responses to corticotropin and basal plasma aldosterone or renin and potassium values, between hemodialysis-induced changes in plasma aldosterone and those in potassium or renin; but not between various indexes of heparin treatment and aldosterone activity. Bilateral nephrectomy reduced basal plasma renin and aldosterone concentrations and aldosterone responsiveness in five preoperatively normoreninemic or hyperreninemic patients, but not in a hyporeninemic patient. These results demonstrate the complementary roles of circulating renin and potassium in the control of aldosterone release under basal and stimulatory conditions in patients with terminal renal failure. Administration of heparin in dosages used during long-term hemodialysis does not appear to significantly interfere with aldosterone control.