Objective: To determine if nonpregnant plasma volume is altered in wom
en who are homozygous for the T 235 coding angiotensinogen allele, whi
ch predisposes women to an increased risk of preeclampsia. Methods: We
measured plasma volume by Evans blue dilution and analyzed it as a fu
nction of angiotensinogen genotype in 15 nulligravid women during midf
ollicular phase of 26 menstrual cycles. Eleven women were evaluated du
ring two cycles, and four women were evaluated in one cycle. Fourteen
women were white, and one was Asian. No subjects had illnesses or were
taking medication. The range of body mass index (BMI [kg/m(2)]) was 2
0.2-31.0. Plasma volume (mL) was reported as plasma volume divided by
BMI to control for variations in body sizes. Statistical analysis was
performed by analysis of variance with post hoc testing using Fisher l
east significant difference test for multiple comparisons (P < .05 acc
epted for significance). Results: Angiotensinogen genotype analysis sh
owed five women homozygous for M 235, three women homozygous for T 235
, and seven women who were heterozygous (MT 235). T 235 homozygotes ha
d significantly lower plasma volume divided by BMI compared with women
who were homozygous for M 235 and women who were heterozygous for MT
235 (mean + standard deviation [SD] [71.2 +/- 8.8, 86.6 + 5.2, 95.8 15.6, respectively, P < .05]). There was a tendency toward higher plas
ma volume in heterozygote MT 235 compared with homozygote M 235 carrie
rs, but it was not statistically significant. Conclusion: We conclude
that the homozygous T 235 coding angiotensinogen genotype is associate
d with reduced plasma volume in nulligravid women during the follicula
r phase of the menstrual cycle compared with M 235 homozygotes and het
erozygotes. This association of the T 235 coding genotype might contri
bute to fetal growth restriction in preeclampsia. (Obstet Gynecol 1998
;92:171-3. (C) 1998 by The American College of Obstetricians and Gynec
ologists.)