Figure 45

Control of mineralocorticoid production. A, Control of aldosterone production under normal circumstances. A decrease in renal perfusion pressure or tubular sodium content (1) at the level of the juxtaglomerular apparatus and macula densa of the kidney triggers renin release (2). Renin acts on its substrate angiotensinogen to generate angiotensin I, which is converted rapidly by angiotensin-converting enzyme to angiotensin II. Angiotensin II then induces peripheral vasoconstriction to increase perfusion pressure (6) and acts on the zona glomerulosa of the adrenal cortex (3) (see Fig. 4-2) to stimulate production and release of aldosterone (4). Potassium and adrenocorticotropic hormone (ACTH) also play a minor role in aldosterone production in some circumstances. Aldosterone then acts on the cells of the collecting duct of the kidney to promote reabsorption of sodium (and passively, water) in exchange for potassium and hydrogen ions excreted in the urine. This increased secretion promotes expansion of extracellular fluid volume and an increase in renal tubular sodium content (5) that further suppresses renin release, thus closing the feedback loop (servomechanism). B, Abnormalities present in primary aldosteronism. Autonomous hypersecretion of aldosterone (7) leads to increased extracellular fluid volume expansion and increased renal tubular sodium content. These elevated levels are a result of increased renal sodium and water reabsorption (8) at the expense of increased potassium and hydrogen ion excretion in the urine. The increase in sodium and volume then increase systemic blood pressure and renal perfusion pressure and sodium content (9), thereby suppressing further renin release (10) and angiotensin II production (11). Thus, in contrast to the normal situation depicted in panel A, the levels of angiotensin II are highly suppressed and therefore do not contribute to an increase in systemic blood pressure (12). In primary aldosteronism, ACTH (13) has a dominant modulatory role in influencing aldosterone production and hypo-kalemia, resulting from increased urinary potassium exchange for sodium, which has a negative effect on aldos-terone production (14).

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