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The renin-angiotensin-aldosterone system (RAAS) helps regulate
blood pressure, blood volume, and fluid and electrolyte balance. The system can mediate cardiovascular pathology.
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Angiotensin II is formed by the actions of two enzymes:
renin and angiotensin-converting enzyme (ACE).
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Angiotensin II causes
asoconstriction (primarily in arterioles) and release of aldosterone.
In addition, angiotensin II can promote pathologic changes in the heart and blood vessels.
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Aldosterone acts on the
kidneys to promote retention of sodium and water.
In addition, aldosterone can also mediate pathologic changes in cardiovascular function.
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ACE inhibitors are used to treat patients with
hypertension, heart failure, myocardial infarction (MI), and nephropathy, both diabetic and nondiabetic.
In addition, they are used to prevent MI, stroke, and death (from cardiovascular causes) in patients at high risk for a cardiovascular event.
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By suppressing aldosterone release, ACE inhibitors can cause
hyperkalemia
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ARBs are similar to ACE inhibitors in that they cause
vasodilation, suppress aldosterone release, promote excretion of sodium and water, reduce blood pressure, and cause birth defects and angioedema.
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By blocking angiotensin II receptors on blood vessels, ARBs cause
dilation of arterioles and veins.
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ARBs differ from ACE inhibitors in that they do not cause
hyperkalemia or cough.
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