Stimulation of aldosterone by ACTH in normal and hypertensive pregnancy

The observation that plasma renin (PRC) is suppressed to a greater degree than aldosterone (Paldo) concentration in preeclampsia has led us to examine the role of nonangiotensin factors in the control of aldosterone release in pregnancy. The aim of this study was to determine whether the aldosterone response to adrenocorticotrophic hormone (ACTH) was altered in normal or preeclamptic pregnancy. After 4 days of a 100 mmollday sodium diet, serum cortisol, PRC, and Paldo were measured every 20 min during an incremental low-dose ACTH infusion (over 80 min) in 10 nonpregnant, nine normal pregnant, and nine preeclamptic women. Baseline PRC, Paldo, and cortisol were significantly higher in normal pregnant than in nonpregnant women (P< .05), but serum ACTH concentration was similar. Following ACTH infusion there was significant stimulation of cortisol in both groups (P< .001) and the maximum rise (963[824,1163] nmol/L, median [interquartile range]) was greater in pregnant than in nonpregnant women (507[402,837]), P< .01. Plasma aldosterone also rose significantly following ACTH in both groups (P< .01) and the maximum rise was also greater in normal pregnant (1186[828,2609] fmol/mL) than nonpregnant women (874[598,1065]), P= .05. These changes were not related to basal cortisol or aldosterone concentrations in either group. Baseline PRC was significantly lower in preeclamptic than in normal pregnant women (P< .05) but Paldo, serum ACTH, and cortisol concentrations did not differ significantly. Following ACTH there was significant stimulation of cortisol in both groups (P<.001) and the maximum increment in preeclamptic women following ACTH infusion (807[708,1007] nmol/L) was similar to that of normal pregnant women. Plasma aldosterone did not change significantly during ACTH infusion in preeclamptic women (P = .20) and the maximum increment in Paldo (531[219,1165]) was reduced significantly compared with normal pregnant women. Blood pressure was not altered by these infusions. Normal pregnant women have a heightened cortisol and aldosterone response to ACTH. Although this cortisol response is intact in preeclampsia, the aldosterone response is reduced considerably. This reduced aldosterone response to ACTH in preeclampsia may contribute to the lower basal Paldo of preeclamptic pregnancy