Abstract
In several animal species and in man, ACTH and angiotensin II seem to be the most important regulatory factors of corticosteroid secretion. Chronic overproduction of ACTH results in increased Cortisol and adrenal androgen secretion (Cushing’s disease), while aldosterone levels are usually normal or suppressed [1]. Chronic overproduction of angiotensin II, either physiologic (e.g. sodium deficiency) or pathologic (e.g. renin-producing kidney tumor or renal artery stenosis) leads to increased plasma and urinary aldosterone levels, but signs of hypercortisolism are absent. Short-term administration of ACTH produces a rise in plasma Cortisol and aldosterone levels [2], while short-term infusions of angiotensin II increase plasma aldosterone, but not plasma Cortisol [3]. In adrenal cell suspensions derived from animals or man, ACTH stimulates Cortisol as well as aldosterone secretion, and even angiotensin II, besides its effect on aldosterone secretion, stimulates Cortisol release [4–7].
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Oelkers, W., Schöneshöfer, M., Schultze, G., Fuchs-Hammoser, R., Venema, F. (1980). Interactions Between Angiotensin II and ACTH on the Human Adrenal Gland. In: Philipp, T., Distler, A. (eds) Hypertension: Mechanisms and Management. International Boehringer Mannheim Symposia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67712-0_19
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DOI: https://doi.org/10.1007/978-3-642-67712-0_19
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