作者: S. Alwan , J.E. Polifka , J.M. Friedman
DOI: 10.1002/BDRA.20102
关键词:
摘要: Angiotensin II (A-II) is the main effector of renin-angiotensin system. A-II functions by binding its type 1 (AT1) receptors to cause vasoconstriction and retention sodium fluid. Several AT1 receptor antagonists-a group drugs collectively called "sartans"-have been marketed during past few years for treatment hypertension heart failure. At least 15 case reports describe oligohydramnios, fetal growth retardation, pulmonary hypoplasia, limb contractures, calvarial hypoplasia in various combinations association with maternal losartan, candesartan, valsartan, or telmisartan second third trimester pregnancy. Stillbirth neonatal death frequent these reports, surviving infants may exhibit renal damage. The abnormalities, which are strikingly similar those produced angiotensin-converting enzyme (ACE) inhibitors trimesters pregnancy, probably related extreme sensitivity fetus hypotensive action drugs. Very little information available regarding outcome human pregnancies mother was treated an antagonist first trimester, but animal studies have not demonstrated teratogenic effects after large doses antagonists organogenesis. We conclude that pharmacological suppression system through ACE inhibition blockade seems disrupt vascular perfusion function. recommend be avoided pregnancy women who become pregnant while taking one medications changed antihypertensive drug a different class as soon recognized.