Adverse Reactions
Dizziness, headache, upper-respiratory- tract infection, cough, and gastrointestinal disturbances have been reported with AT-II-receptor antagonists at about the same rates as with placebo. All AT-II-receptor antagonists are less likely than ACE inhibitors to cause cough. Thus, it may be clinically advantageous to use an AT-II-receptor antagonist in patients who develop ACE inhibitor-induced dry cough.
Intravascular volume and renal function depend in part on the RAS. Patients who are volume depleted, are being treated aggressively with diuretics, are hyponatremic, or have progressive renal insufficiency or renal artery stenosis are at a greater risk of hypotension and deterioration of renal function. Therapy with AT-II-receptor antagonists in patients with these conditions should be initiated at a reduced dosage, or the underlying condition should first be corrected.
Like ACE inhibitors, AT-II-receptor antagonists may induce hyperkalemia in patients with chronic renal failure and in those receiving potassium-sparing diuretics or potassium supplements. Although hyperkalemia and renal insufficiency are more likely to occur in certain at-risk patients (e.g., patients with severe congestive heart failure), serum potassium and renal function must be monitored in all patients. However, in clinical trials of AT-II-receptor antagonists, clinically important changes in serum potassium levels were reported for valsartan only.
AT-II-receptor antagonists, like ACE inhibitors, are contraindicated in pregnant women and those who may become pregnant because direct action on the RAS can cause fetal morbidity and death.
Am J Health Syst Pharm. 2000;57(13) © 2000 American Society of Health-System Pharmacists
Cite this: Angiotensin II-Receptor Antagonists: An Overview - Medscape - Jul 01, 2000.
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