Basal Plasma Aldosterone Levels Research Articles

Responsiveness of plasma aldosterone: Dependency upon basal secretory activity

The responsiveness of plasma aldosterone levels to various stimuli was evaluated in 44 normal subjects, 17 patients with mild to moderate renal failure, 30 patients with terminal renal failure, and 13 anephric subjects. Plasma aldosterone, renin activity (PRA), cortisol, sodium, and potassium levels were measured before and after one hour of upright posture (N = 191); ACTH infusions (N = 76); and angiotensin II infusion (N = 36). Plasma aldosterone responses correlated (r greater than or equal to 0.53; p less than 0.02) with basal plasma aldosterone levels during upright posture in all four groups, with ACTH infusion in all groups except anephric subjects, and with angiotensin II administration in patients with mild to moderate renal failure or patients combined. These relationships were consistently closer than those between aldosterone responses and changes in PRA or basal PRA. However, postural aldosterone responsiveness at any given basal aldosterone level was significantly lower in patients with renal disease than in normal subjects, and this was associated with a parallel impairment in renin responsiveness. In contrast, when related to basal levels aldosterone responsiveness to ACTH or angiotensin II appreared to be comparable in normal subjects and patients with renal disease. Aldosterone responses to posture, ACTH, or angiotensin II did not correlate with associated changes in plasma cortisol, sodium, or potassium levels. These data suggest that basal adrenal secretory activity is a major factor conditioning aldosterone responsiveness to various stimuli in normal subjects as well as in patients with renal disease.

Effect of spironolactone on urinary excretion of immunoreactive prostaglandin E in essential hypertension and primary aldosteronism.

To determine the effect of aldosterone antagonist on renal prostaglandin E synthesis, the rate of urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically before and during the oral administration of an aldosterone antagonist, spironolactone, in 5 patients with essential hypertension, 3 with primary aldosteronism and 2 with postoperative primary aldosteronism. Spironolactone was administered at an oral dose of 25 mg 4 times daily for about 1 week. In the control state, the rates of urinary prostaglandin E excretion ranged from 151 ng/day to 4,527 ng/day in essential hypertension. The rates were not augmented in primary aldosteronism but decreased after the removal of an aldosterone producing adenoma. No obvious relationship was observed between plasma aldosterone concentration and the rate of urinary prostaglandin E excretion. On the first day of spironolactone administration, the excretion rates of urinary prostaglandin E were markedly increased independently of basal plasma aldosterone level in all cases except one case of essential hypertension. Urinary prostaglandin E excretion was increased with the concominant increase of urinary Na/K ratio in essential hypertension and primary aldosteronism. After the second day, the augmented urinary prostaglandin E excretion was decreased and the changes of urinary prostaglandin E excretion varied from case to case. These results suggest that synthesis of renal prostaglandin E is not mainly regulated by aldosterone in essential hypertension and primary aldosteronism.

Hypokalemic Crisis Simulating Intestinal Obstruction in a 4-Year-Old Girl

A 4-year-old girl had abdominal distention, muscular weakness, renal tubular dysfunction, and hypertension associated with hypokalemic metabolic alkalosis. There were no clinical symptoms of cortisol deficiency, but there was excessive deoxycorticosterone and cortisocsterone production. Basal plasma aldosterone levels were undetectable; however, adrenocorticotropic hormone (ACTH) stimulation brought plasma aldosterone levels up to normal. The urinary pregnanediol, tetrahydro-deoxycorticosterone (THDOC), and tetrahydrocorticosterone (THB) concentrations were elevated. Stimulation of ACTH failed to increase urinary 17-ketosteroid, 17-hydroxycorticosteroid, or plasma cortisol levels significantly, while urinary THDOC, THB, and plasma corticosterone concentrations were further elevated. The elevated plasma corticosteroid intermediates were suppressed by dexamethasone administration. When physiologic doses of dexamethasone were administered, the hypertension, electrolyte imbalance, and abnormal corticosteroid secretion were all corrected. The studies indicated a partial 17alpha-hydroxylase defect in this patient.

Secretory Regulation and Episodic Secretion of Aldosterone in Patients with Primary Aldosteronism

In nine patients with primary aldosteronism (PA), plasma aldosterone was measured in order to evaluate a role of the renin-angiotensin system, ACTH and potassium in the secretion of aldosterone. The circadian rhythm and the episodic secretion were also studied in three patients. The results were as follows: 1) In seven out of nine patients, plasma aldosterone levels (PAL) decreased after the two-hours standing, and it run parallel with plasma cortisol levels (PCL), but not with plasma renin activity (PRA). 2) An intravenous infusion of saline of 2000 ml during four hours failed to suppress PAL in all of five patients and the change of PAL was parallel with that of PCL. 3) PAL decreased markedly after the oral administration of 1 mg of dexamethasone (Dexa), and there was a significantly positive correlation (r = 0.898, p less than 0.01) between basal PAL and the its decrement. 4) Following an intravenous infusion of angiotensin-II at a rate of 0.015 microgram/Kg/min after the pretreatment with Dexa, no significant increase of PAL was observed in any of the five patients. 5) Following a single injection of 0.25 mg of ACTH after the pretreatment with Dexa, PAL rose rapidly, and its peak level was found 60 minutes after the injection. In four out of eight patients this rise was greater than that in the normal subjects. 6) An intravenous infusion of 20 mEq of KCl after the pretreatment with Dexa, produced normal response i.e., an increase of PAL in all seven of the patients. 7) The circadian rhythm and the episodic secretion of PAL in the patients were synchronous with those of PCL throughout twenty four hours.

Congenital adrenal hypoplasia: An isolated defect of organogenesis

Data are presented on four boys, including three siblings, two of whom were identical twins who had clinical, biochemical, and hormonal features of congenital adrenal hypoplasia. One twin died and at necropsy a macroscopically normal pituitary was found, but adrenal tissue could not be identified. Normal plasma levels of growth hormone, thyroid-stimulating hormone, and luteinizing hormone appropriate for the degree of sexual maturation were demonstrated in the two involved siblings of this twin. Insulin-induced hypoglycemia caused a prompt and adequate rise in, plasma adrenocorticotropic hormone levels without a concomitant rise in plasma cortisol levels. The basal plasma aldosterone levels were low and failed to increase following the stimulus of erect posture. Adrenal hypoplasia in these patients represents an isolated defect of organogenesis without demonstrable disturbance in anterior pituitary Data are presented on four boys, including three siblings, two of whom were identical twins who had clinical, biochemical, and hormonal features of congenital adrenal hypoplasia. One twin died and at necropsy a macroscopically normal pituitary was found, but adrenal tissue could not be identified. Normal plasma levels of growth hormone, thyroid-stimulating hormone, and luteinizing hormone appropriate for the degree of sexual maturation were demonstrated in the two involved siblings of this twin. Insulin-induced hypoglycemia caused a prompt and adequate rise in, plasma adrenocorticotropic hormone levels without a concomitant rise in plasma cortisol levels. The basal plasma aldosterone levels were low and failed to increase following the stimulus of erect posture. Adrenal hypoplasia in these patients represents an isolated defect of organogenesis without demonstrable disturbance in anterior pituitary