EFFECT OF PREGNANCY ON THE HYPOTENSIVE ACTION OF ANGIOTENSIN – CONVERTING ENZYME INHIBITORS IN FEMALE RATS

Abstract

The effect of angiotensin-converting enzyme (ACE) inhibitors versus alpha methyldopa on the arterial blood pressure of pregnant adult female rats were studied. Captopril, enalapril, benazepril and perindopril were injected intraperitoneally and used as representative for the commonly used antihypertensive ACE inhibitors. The effects of ACE inhibitors and alpha methyldopa on estradiol, porgesterone, prolactin, cortisol, cholesterol, glucose, potassium and calcium blood levels were studied. Results showed that pregnancy significantly increased both the intensity and duration of the hypotensive effect of ACE inhibitors in comparison with the non pregnant rats. This difference in the effect was not observed in case of alpha methyldopa. Pregnancy per se significantly increased the blood levels of estradiol, progesterone, prolactin, cortisol and glucose . Both estradiol and progesterone were increased directly after occurrence of pregnancy. While cortisol, prolactin and glucose levels were increased after 12 days of starting of pregnancy. Alpha methyldopa significantly increased the blood levels of estradiol, progesterone and prolactin while decreased that of cortisol. Perindopril significantly increased the blood levels of both estradiol and progesterone after 18 days of gestation . Benazepril induced significant reduction of both estradiol and prolactin while increased that of progesterone. Both alpha methyldopa and benazepril significantly increased the glucose blood levels. Captopril, enalapril, and benazepril significantly increased the potassium blood levels after 12 days of starting of gestation, however, both alpha methyl dopa and perindopril did not. While captopril significantly decreased the calcium blood level, alpha methyldopa significantly increased it. In conclusion, pregnancy per se potentiates the hypotensive effect of ACE inhibitors but not that of alpha methyldopa. This may be, in part due to elevation of female sex hormones and refractoriness to angiotensin II (Ang II) that occur during pregnancy.