Why the study?
How does the activity of the renin-angiotensin-aldosterone system differ between normal pregnancy and preeclampsia?
How does the activity of the renin-angiotensin-aldosterone system differ between normal pregnancy and preeclampsia?
The renin-angiotensin-aldosterone system shows decreased activity in preeclampsia compared to normal third-trimester pregnancy, which may contribute to altered hemodynamic control.
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RAAS suppression in preeclampsia may underlie hemodynamic changes; leaves open causal and therapeutic roles pending prospective studies.
OBJECTIVE: To evaluate the activity of the renin-angiotensin-aldosterone system in the circulation during the three trimesters of normal pregnancy and in women with preeclampsia. METHODS: Normal pregnant volunteers (n = 7) were studied throughout pregnancy, and women with preeclampsia (n = 8) were studied in the third trimester. Plasma active renin and aldosterone were measured by radioimmunoassay. Angiotensin I and angiotensin II were determined by radioimmunoassay after separation of the peptides by high-performance liquid chromatography. RESULTS: Active renin concentration increased in the first trimester of normal pregnancy, whereas angiotensin I, angiotensin II, and aldosterone remained at a level comparable to the postpartum values. Highest activity of the renin-angiotensin-aldosterone system was observed during the third trimester with increased levels of angiotensin I, angiotensin II, and aldosterone. In contrast, in patients with preeclampsia, despite a slight increase of active renin levels, the other parameters of the renin-angiotensin-aldosterone system were low compared with the third trimester of normal pregnancy and were comparable to postpartum data. CONCLUSION: Our results suggest that during the first trimester of normal pregnancy, active renin concentration in the plasma is increased and that renin is not the factor that limits angiotensin II synthesis. These results also confirm decreased activity of the renin-angiotensin-aldosterone system in preeclampsia. This could contribute to the diminished hemodynamic control observed in pregnant women developing preeclampsia.
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B. Langer (1998) studied this question.
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