Plasma renin activity (PRA) is measured as part of the diagnosis and treatment of hypertension.
Patients with primary hyperaldosteronism will have an increased aldosterone (for more information see the aldosterone test) production associated with a decreased PRA. Patients with secondary hyperaldosteronism (that is, caused by renal disease or renal vascular disease) will have increased plasma levels of renin and aldosterone.
Patients may also have renin and aldosterone levels checked in essential hypertension to evaluate if patients are salt sensitive. This will cause a low renin with normal aldosterone levels, and this helps to guide the physician in choosing the correct medication for these patients. Patients with low renin hypertension, who are salt sensitive, respond well to diuretic medications.
Renin is an enzyme released by specialized cells of the kidney into the blood. It is in response to sodium depletion and/or low blood volume. Renin converts angiotensinogen (a protein released into the blood by the liver) to angiotensin I.
Angiotensin I is converted to angiotensin II by an enzyme in the veins of the lungs. Angiotensin II acts on the adrenal cortex to stimulate the release of aldosterone. Aldosterone acts on the distal tubules of the kidneys to decrease the loss of sodium ions and secondarily fluid. This has the effect of increasing blood pressure. In addition, angiotensin causes constriction of small blood vessels, which also increases blood pressure.
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