Why the study?
Does ACTH and AIII infusion stimulate aldosterone secretion differently in normal subjects compared to patients with primary aldosteronism or renal failure?
Does ACTH and AIII infusion stimulate aldosterone secretion differently in normal subjects compared to patients with primary aldosteronism or renal failure?
Patients with primary aldosteronism demonstrate a lower threshold for ACTH-stimulated aldosterone secretion compared to normal subjects and those with renal failure.
May support refined ACTH testing thresholds in primary aldosteronism; leaves open effects on diagnosis and management.
ACTH and des-Asp1-angiotensin II (AIII) can raise plasma aldosterone. To assess the threshold for ACTH and AIII stimulated adrenal steroidogenesis we infused ACTH (from 0.03 to 10 ng ACTH/min) and AIII (from 0.1 to 20 ng/kg/min) to dexamethasone pretreated sodium deplete normal subjects and patients with primary aldosteronism, chronic renal failure, and end stage renal disease maintained with continuous ambulatory peritoneal dialysis. Plasma aldosterone in the primary aldosteronism group increased significantly at 0.3 ng ACTH/min compared with 1 to 3 ng ACTH/min in all other groups. The threshold dose for an ACTH stimulated rise in plasma aldosterone was as at least as low as the dose necessary to raise cortisol in all groups. The threshold dose for an AIII stimulated rise in plasma aldosterone was 4 ng/kg/min in normals and between 1 and 3 ng/kg/min in primary aldosteronism. The metabolic clearance rate (MCR) of aldosterone was determined by constant infusion of [3H]-aldosterone. The decline in MCR during AIII infusion contributed less than 15% to the rise in plasma aldosterone in normals and patients with primary aldosteronism.
No takes yet. Share an insight, caveat, or question.
Zager et al. (1982) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: