(Hypertension. 1995;26:1019-1023.)
© 1995 American Heart Association, Inc.
Articles |
From the Departments of Obstetrics and Gynecology, Pediatrics, and Center for Medical Research, School of Medicine, Catholic University of Chile, Santiago.
Abstract We conducted the present study to investigate
whether the vasodilator nitric oxide plays a role in plasma
volume homeostasis during pregnancy. Pregnant
Sprague-Dawley rats were randomly assigned to a control
group (n=18) or to groups receiving 0.69 mmol/L (n=11) or 1.7 mmol/L
(n=14) N
-nitro-L-arginine, a
competitive inhibitor of nitric oxide synthetase, from
gestational days 7 through 21. On day 20 systolic pressure was
measured. On day 21 blood samples were taken for plasma volume,
hematocrit, and hormonal measurements. Fetal and placental weights also
were determined. Systolic pressure was significantly higher in
experimental rats (101±6 and 115±6 mm Hg in the 0.69 and 1.7 mmol/L
groups, respectively) than in controls (79.7±7.5 mm Hg), and plasma
volume was lower (18.4±1.1 and 17.1±0.5 mL) than in controls
(21.5±0.8 mL). Both experimental groups had increased hematocrit
levels. Plasma renin activity was significantly lower in the
experimental groups (11.5±3 and 7.2±1.5 ng angiotensin
I/mL per hour) than in controls (21.9±2.7 ng angiotensin
I/mL per hour); however, no changes were observed in
aldosterone levels. Experimental groups had lower fetal
weight (4.6±0.1 and 5.1±0.1 g) than controls (5.5±0.1 g). In
addition, fetal hindlimb hypoplasia was observed in the experimental
groups. In conclusion, the present data indicate that long-term
N
-nitro-L-arginine administration
to pregnant rats leads to increased blood pressure, reduced plasma
volume expansion, lower plasma renin activity, and fetal growth
retardation. These results suggest that nitric oxide may play an
important role in maternal systemic vasodilatation and indirectly in
plasma volume homeostasis and fetal growth.
Key Words: pregnancy nitric oxide aldosterone renin fetal growth retardation
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