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Effect of hydrogen ion concentration on corticosteroid secretion
The American Journal of Physiology
|March 11, 1986
Summary
Extracellular hydrogen ion (H+) concentration directly impacts adrenal corticosteroid secretion. Alkalosis inhibits aldosterone secretion, while H+ levels correlate with aldosterone and other steroid hormone release in response to ACTH.
Area of Science:
- Endocrinology
- Physiology
- Acid-Base Balance
Background:
- Corticosteroid secretion is regulated by various factors, including adrenocorticotropic hormone (ACTH).
- The direct influence of acid-base balance on adrenal steroidogenesis is not fully understood.
- Understanding these mechanisms is crucial for managing endocrine and metabolic disorders.
Purpose of the Study:
- To investigate the direct effects of extracellular hydrogen ion (H+) concentration on corticosteroid secretion.
- To determine how changes in acid-base balance influence basal and ACTH-stimulated hormone release from the canine adrenal gland.
Main Methods:
- Isolated, perfused canine adrenal glands were used to control perfusate composition.
- Extracellular H+ concentration was manipulated by altering partial pressure of carbon dioxide (PCO2) or bicarbonate ([HCO3-]) levels.
- Secretion of aldosterone, corticosterone, 18-hydroxycorticosterone, and cortisol was measured under basal and ACTH-stimulated conditions.
Main Results:
- Alkalosis significantly inhibited ACTH-stimulated aldosterone secretion.
- A positive correlation was observed between H+ concentration and aldosterone secretion, but a negative correlation with corticosterone and 18-hydroxycorticosterone secretion in response to ACTH (pH range 7.19-7.85).
- Neither acidosis nor alkalosis directly affected basal or ACTH-stimulated cortisol secretion.
Conclusions:
- Extracellular H+ concentration directly modulates ACTH's effect on aldosterone secretion via the adrenal cortex.
- Acid-base disturbances specifically impact the zona glomerulosa in canine adrenal glands.
- H+ concentration may influence late stages of aldosterone biosynthesis.