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Renin-aldosterone relationships in pregnancy-induced hypertension.

Authors
  • Brown, M A1
  • Zammit, V C
  • Mitar, D A
  • Whitworth, J A
  • 1 Department of Renal Medicine, St. George Hospital, University of New South Wales, Sydney, Australia.
Type
Published Article
Journal
American journal of hypertension
Publication Date
June 1992
Volume
5
Issue
6 Pt 1
Pages
366–371
Identifiers
PMID: 1524761
Source
Medline
License
Unknown

Abstract

The relationship between plasma renin (PRC) and aldosterone (PAC) concentrations was determined in 83 normal third trimester pregnant women (P), 50 women with pregnancy-induced hypertension (PIH), and 80 age-matched nonpregnant women not taking oral contraceptives (NP). Normal pregnant women had a slightly higher 24-h urine sodium: creatinine ratio than the other groups (P less than .001) (NP: 10 +/- 4 v P: 15 +/- 8 v PIH: 12 +/- 7; mean +/- SD). Both PRC and PAC were higher in normal pregnant women as was the ratio PAC:PRC [normal pregnant 195 (158 to 337) v nonpregnant 130 (101 to 209), median (interquartile range); P less than .001]. This was accompanied by a slightly reduced slope (sensitivity) of the logPRC-logPAC relationship in normal pregnant women (P less than .05). Women with PIH had reduced PRC and PAC compared with normal pregnant women but a two-fold greater increase in PAC:PRC ratio [PIH 411 (277 to 598) v normal pregnancy 195 (158 to 337), P less than .001], with a rise in the slope (sensitivity) of the logPRC-logPAC relationship in women with PIH (P less than .001). Thus there is proportionately greater aldosterone release in the third trimester of normal pregnancy than in nonpregnant women. This preferential increase in aldosterone may be due to altered adrenal sensitivity to angiotensin II or may reflect enhanced nonangiotensin stimulation of aldosterone during pregnancy. Women with PIH have reduced PRC and PAC but relatively greater stimulation of aldosterone than normal pregnant women, possibly due to enhanced sensitivity of the adrenal glands to angiotensin II.

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