The Influence of Normotensive Pregnancy and Pre‐Eclampsia on Angiotensin‐Converting Enzyme

Abstract

Serum angiotensin-converting enzyme (SACE) levels were determined in normotensive pregnant subjects and patients with pre-eclampsia in the third trimester of pregnancy and 5 days, 3 and 6 months after parturition, and also in the first and second trimester in the normotensive group. SACE levels were reduced during pregnancy and 5 days after delivery in the normotensive subjects compared with the levels 3 and 6 months after delivery and to the non-pregnant control subjects. After correction for plasma volume expansion, SACE was reduced in first and second trimester only. In pre-eclampsia both SACE and corrected SACE were significantly lower in third trimester and 5 days after parturition than 3 and 6 months after delivery and in non-pregnant control subjects. The reason for the reduced level of SACE in first and second trimester during normal pregnancy is not known. The low SACE levels in pre-eclampsia may be a secondary phenomenon due to a decreased placental synthesis without primary importance for the blood pressure regulation.

Angiotensin converting enzyme activity in hypertensive pregnancy

“…A comparable investigation of ACE activity in 16 hypertensive gravidas at 36 weeks' gestation and 17 normotensive women at 40 weeks' gestation was performed by RASMUSSEN et al [8]. Serum levels of ACE activity in the hypertensive group of RASMUSSEN and colleagues [8] were very similar to those found in the 16 subjects with PIH in the current study, 20 ± 3 vs 21 ±4 units, respectively.…”

“…This enzyme catalyzes the conversion of angiotensin I to angiotensin II, a potent vasopressor and deactivates a vasodepressor, bradykinin, thereby raising blood pressure. Vascular endothelium is the primary source of ACE [2,8,9] and it can be measured in plasma or serum. Studying 18 normotensive primigravida, OATS et al [7] found ACE levels to be significantly lowered during normotensive pregnancy and to be dependent on gestational duration.…”

Renin-angiotensin-aldosterone system in pregnancy-induced hypertension

“…[10][11][12] Another failed to find any difference in ACE activity between them. 13 Contrary to these results, we hypothesize that if plasma ANG II levels, plasma renin substrate and plasma renin concentration are all decreased in the third trimester in women with pregnancyinduced hypertension, it is likely that ANG II biosynthesis (ACE activity) also be altered in the same direction. To clarify this controversy, we measured two of the components of the reninangiotensin-aldosterone system (RAA system): plasma ACE activity and plasma aldosterone concentration in third trimester women with PIH and those without PIH.…”

Constancy of serum angiotensin-converting enzyme activity in normal and complicated pregnancy

“…OATS, et al [7] prospectively evaluated multiple samples for SACE activity in 18 normal primigravidae and concluded that enzyme activity was depressed during normal pregnancy, but rose as pregnancy advanced into the third tri-mester, and returned to non-pregnant levels by 6 weeks postpartum. RASMUSSEN, et al [9] found that normotensive pregnant subjects studied during pregnancy arid 5 days post-partum had lower SACE activity compared to their own levels 3 to 6 months following delivery or to a group of non-pregnant control women.…”