Upregulation of endothelial and neuronal constitutive nitric oxide synthase in pregnant rats. Xu, Ding-Li, Pierre-Yves Martin, Judy St John, Phoebe Tsai, Sandra N Summer, Mamiko Ohara, Jin K Kim, Robert W Schrier. Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
APStracts 3:0269R, 1996.
Pregnancy is characterized by hemodynamic and body fluid alterations. Increased NO production has been suggested to play a role in the hemodynamic alterations of pregnancy and has also been reported to increase arginine vasopressin (AVP) release. We therefore hypothesized that gestation could increase both nitric oxide synthase (NOS) constitutive isoforms, neuronal NOS and endothelial NOS, and thereby contribute to the hypoosmolality and peripheral arterial vasodilation of pregnancy, respectively. The present study therefore was undertaken to examine the constitutive NOS isoforms in aortas, mesenteric arteries, and hypothalami of pregnant rats on the day 20 of gestation as compared with age-matched non-pregnant rats. Plasma AVP was determined by radioimmunoassay and hypothalamic mRNA AVP by solution hybridization assay. Hypothalamic neuronal NOS was assessed by Northern blot and Western blot, whereas endothelial NOS was assessed by Western blot in arteries and hypothalamus. The results demonstrated that: 1) Plasma AVP and hypothalamic AVP mRNA are increased in pregnant rats (n=8); 2) nNOS protein and mRNA are increased in hypothalamus of pregnant rats (n=4), and 3) eNOS expression, using Western blot analysis, is increased in both conductance (aorta) as well as resistance (mesenteric) arteries of pregnant rats (n=4). We conclude that both of the constitutive NOS isoforms are increased in pregnant rats, suggesting that the peripheral arterial vasodilation and hypoosmolality of pregnancy could be mediated by these isoforms.

Received 29 January 1996; accepted in final form 14 June 1996.
APS Manuscript Number R59-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996