Conversely spironolactone therapy is associated with a greater increase in aldosterone production. We have observed that therapy with a thiazide diuretic results in a reduction of serum potassium and a greater increase in renin activity than therapy with the potassium-retaining diuretic, spironolactone, despite comparable natriuretic responses with both drugs.
In patients with essential hypertension, diuretic induced alterations in serum potassium concentrations may affect both renin and aldosterone secretion. Small changes in plasma potassium have a greater effect on aldosterone than on renin secretion. Conversely, hypokalemia inhibits aldosterone production. The renin enzyme circulates in the bloodstream and hydrolyzes (breaks down) angiotensinogen secreted from the liver into the peptide angiotensin I. This effect of potassium on aldosterone serves as a protective mechanism against the development of hyperkalemia. Plasma renin activity (PRA) is measured as part of the diagnosis and treatment of hypertension (high blood pressure). In contrast, increases of plasma potassium directly stimulate aldosterone secretion. Renin secretion tends to be inhibited by hyperkalemia and stimulated by potassium depletion. Alterations in plasma potassium concentration have opposite and independent effects on renin secretion by the kidney and on aldosterone secretion by the adrenal gland. In general, normal levels include: 1 to 12 months old: 5.8 110.0 nanograms per deciliter (ng/dL). Angiotensin II does more than increase blood volume. The big news, though, was that instead of having low Ang II levels, the low blood volume and low-flow POTS patients had dramatically increased Ang II levels (2-3 times normal), as well as low renin levels. The renin-aldosterone system contributes to the regulation of arterial pressure and to the maintenance of sodium and potassium balance. The normal range for aldosterone levels in your blood varies based on age. Very high levels of Ang II may be wreaking havoc in POTS and ME/CFS.
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