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1 Division of Renal Diseases and Hypertension and 2 Cardiovascular-Pulmonary Research Laboratory, Departments of 3 Medicine and 4 Physiology, University of Colorado School of Medicine, Denver, Colorado 80262
The chronic role of nitric oxide
(NO), independent of prostaglandin synthesis, in the primary peripheral
vasodilation, increased glomerular filtration rate (GFR), and renal
plasma flow (RPF) in normal pregnancy remains to be defined. The
purpose of the present study was to chronically inhibit NOS to return
systemic vascular resistance (SVR), cardiac output (CO), GFR, and RPF
to nonpregnant values. Pregnant rats received the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methyl ester
(L-NAME), orally from gestational days 7 through
14. Results were compared with nonpregnant and untreated
pregnant rats. At 14 days gestation, CO significantly increased in
pregnant vs. nonpregnant rats (187 ± 17 vs. 125 ± 10 ml/min, P < 0.05) as SVR decreased (0.64 ± 0.08 vs. 1.08 ± 0.08 mmHg · ml
1 · min,
P < 0.05) and mean arterial pressure was unchanged
(117 ± 5 vs. 125 ± 2 mmHg, not significant). Pregnant rats
also demonstrated increased GFR (3,015 ± 33 vs. 2,165 ± 136 µl/min, P < 0.01) and RPF (7,869 ± 967 vs.
5,507 ± 290 µl/min, P < 0.05) vs.
nonpregnant rats. L-NAME-treated pregnant rats had values
for CO (118 ± 7 ml/min), SVR (1.09 ± 0.07 mmHg · ml1 · min), GFR (2,264 ± 150 µl/min), and RPF (5,777 ± 498 µl/min), which were no
different than nonpregnant animals. In summary, similar to human
pregnancy, primary peripheral vasodilation occurs early in rat
pregnancy. Furthermore, the hyperdynamic circulation and glomerular
hyperfiltration of normal rat midterm pregnancy can be chronically
reversed by NOS inhibition. These findings suggest a role for
endothelial damage and decreased NO in the pathogenesis of preeclampsia.
peripheral arterial vasodilation; normal pregnancy; nitric oxide synthase
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