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Articles in PresS, published online ahead of print November 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00701.2002
Submitted on August 9, 2002
Accepted on November 11, 2002
1 Women's Health Research Center and Cardiovascular Pulmonary Research Lab, University of Colorado Health Sciences Center, Denver, CO, USA; Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO, USA
2 Women's Health Research Center and Cardiovascular Pulmonary Research Lab, University of Colorado Health Sciences Center, Denver, CO, USA
3 Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, CO, USA
4 Women's Health Research Center and Cardiovascular Pulmonary Research Lab, University of Colorado Health Sciences Center, Denver, CO, USA; Department of Anthropology, University of Colorado at Denver, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: lorna.g.moore{at}uchsc.edu.
We tested the hypotheses that pregnancy increases uterine artery (UtA) vasodilator response to flow and that this increase is impaired under conditions of chronic hypoxia (30 da, simulated elev 3960 m). UtA were isolated from 24 normoxic or chronically hypoxic mid-pregnant guinea pigs and studied using pressure myography. Normoxic pregnancy increased UtA flow vasodilator response and protected against a rise in wall shear stress (WSS). Chronic hypoxia opposed these effects, prompting vasoconstriction at high flow and increasing WSS above levels seen in normoxic pregnant UtA. The NOS inhibitor nitro-l-arginine (l-NA) eliminated the pregnancy-associated increase in flow vasodilation in normoxic UtA, suggesting increased NO production was responsible. The considerable residual vasodilation after NOS and cyclooxygenase inhibition implicated endothelial-derived hyperpolarizing factor (EDHF) as an additional contributor to flow vasodilation. L-NA increased flow vasodilation in UtA from chronically hypoxic animals, suggesting that chronic hypoxia may have lowered EDHF or elevated peroxynitrite production. We concluded that flow is a important physiologic vasodilator for the acute and more chronic UtA dimensional changes required to increase uteroplacental blood flow during normal pregnancy. That chronic hypoxia opposes the pregnancy-associated rise in UtA flow vasodilation may be among the mechanisms increasing the incidence of pre-eclampsia and intrauterine growth restriction (IUGR) at high altitude.
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